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Full text of "Archives of neurology and psychiatry from the Pathological Laboratory of the London County Asylums 1.1899"

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Director of the Laboratory and Pathologist to the London County Asylums: 
Physician in charge of Out-Patients , Charing Cross Hospital 



And may be purchased, either directly or through any Bookseller, from 


Agents for the sale of the Publications of the London County Council. 


Relation of Syphilis to Organic Brain Disease and Insanity. Introduc¬ 
tion. By F. W. Mott, M.D., F.R.S. 1 

Brain Syphilis in Hospital and Asylum Practice, with Notes of Sixty 
Cases and Twenty-three Asylum post-mortem Examinations. By 

F. W. Mott, M.D., F.R.S. .7 

Observations upon the Etiology and Pathology of General Paralysis .. 166 

An Investigation of the Condition of the Blood in General Paralysis of 
the Insane. By Howard Green, M.R.C.S., L.R.C.P. .. 204 

On the Amount of Water and Phosphorus contained in the Cerebral 
Hemsphere8 and Spinal Cord in General Paralysis of the Insane and 
in other Conditions. By Wakelin Barratt, M.D. .. .. 207 

Syphilis in General Paralysis of the Insane. By H. W. Lewis, M. R.C.S., 

L. R.C.P.223 

Notes of Twenty-two Cases of Juvenile General Paralysis, with Sixteen 

post-mortem Examinations. By F. W. Mott, M.D., F.R.S... .. 250 

Degenerative Changes in the Posterior Spinal Ganglia and Peripheral 
Cutaneous Nerves in a Case of General Paralysis with Bullous Erup¬ 
tion. By F. W. Mott, M.D., F.R.S., and Hamilton Wright, M.D. .. 328 

A Research on the Condition of the Vagus and Sympathetic Nerves in 
General Paralysis of the Insane. By J. 0. Wakelin Barratt, M.l)., 

B.S., B.Sc.Lond., F.R.C.S.Eng., M.R.C.P.Lond. .. .. .. 332 

Comparative Examination of the Tangential System of Fibres of the 
Inferior Frontal Convolution of the Two Hemispheres in General 
Paralysis. By Hamilton Wright, M.D. .. .. .. 342 

Observations on the Chemistry of Nerve-Degeneration. By F. W. 

Mott, M.D., F.R.S., and J. O. Wakelin Barratt, M.D., F.R.C.S. .. 346 

A Case of Amyotrophic Lateral Sclerosis, with Degeneration of the 
Deeper Cellular Layers of the Cortex, the Tangential Fibre System 
being Intact; Diagnosed as General Paralysis. By F. W. Mott, 

M. D., F.R.S. .. .. .. .. ..359 

Microscopical Examination of the Spinal Cord, Peripheral Nerves and 

Muscles in a Case of Acute Poliomyelitis. Fatal Termination Six¬ 
teen Days from the Onset. By F. W. Mott, M.D., F.R.S. .. .. 365 

Combined Sclerosis with Grave Anaemia. By F. W. Mott, M.D., F.R.S. 377 
Report of a Case of Tabes, with Especial Reference to the Changes in 
the Posterior Root Ganglia. By Redcliffe N. Salaman, B. A.Can tab. 388 
Preliminary Observations on the Etiology of Asylum Dysentery. By 
Herbert E. Durham, M.A., M.B., B.C., F.R.C.S. .. .. 403 

Three Cases of Tumour of the Third Ventricle. By F. W. Mott, M.D., 
F.R.S., and J. O. Wakelin Barratt, M.D., F.R.C.S. .. 417 

A Telangiectasis of the Left Frontal Lobe, with Epileptiform Convul¬ 
sions. By Cecil F. Beadles .. .. 440 




Three Dissimilar Cases of Multiple Lesions of the Central Nervous 
System. By A. F. Tredgold, M.R.C.S., L.R.C.P. .. ... 

Preliminary Communication upon the Changes in the Brain, Spinal 
Cord, Muscles and other Organs found in Persons Dying after Pro¬ 
longed Epileptiform Convulsions. By F. W. Mott, M.D., F.R.S. 

Some Statistics relating to Epilepsy in Hanwell Asylum. By J. R. 
Lord, M.B. 

Alcoholic Atrophy in the Central and Peripheral Nervous System 
of a Woman. By Hamilton Wright, M.D., and Margaret Orange, 
L.S.A.Lond., M.D.Brux. 

The Prevention of Phthisis in the Insane. By Eric France, M.B. 

Observations on the Normal Anatomy of the 9th, 10th, 11th and 12th 
Cranial Nerves. By J. O. Wakelin Barratt, M.D., B.S.Lond., 
F.R.C.S.Eng. .. 










Brain Syphilis in Hospital and Asylum Practice, with Notes of Sixty 
Cases and Twenty - three Asylum post-mortem Examinations. 

Figs. 1-18 ... . 38, 40, 102, 109, 116, 122,’ 124, 125, 126, 

127, 128, 135, 153, 154, 160, 165 

Observations upon the Etiology and Pathology of General Paralysis. 

Plate I. Figs. 1-3 . . 184, 187, 197, 203 

Notes of Twenty-two Cases of Juvenile General Paralysis, with Sixteen 
post-mortem Examinations. Plates II., III. Figs. 1-13 272, 274, 275, 276, 

277, 279, 285, 297, 299, 300, 301, 321 
Degenerative Changes in the Posterior Spinal Ganglia and Peripheral 
Cutaneous Nerves in a Case of General Paralysis with Bullous 
Eruption. Plate IV. Figs. 1,2... ... ... ... 329,330 

A Research on the Condition of the Vagus and Sympathetic Nerves in 
General Paralysis of the Insane. Figs. 1-4 ... ... 333, 336, 339 

Observations on the Chemistry of Nerve-Degeneration. Fig. 1 ... 358 

A Case of Amyotrophic Lateral Sclerosis, with Degeneration of the 
Deeper Cellular Layers of the Cortex, the Tangential Fibre System 
being intact; Diagnosed as General Paralysis. Figs. 1-4 861, 362, 363, 364 
Microscopical Examination of the Spinal Cord, Peripheral Nerves and 
Muscles in a Case of Acute Poliomyelitis. Fatal Termination Six¬ 
teen Days from the Onset. Figs. 1-5 ... ... 366, 368, 369, 371, 372 

Combined Sclerosis with Grave Ansemia. Plate V. Figs. 1, 2...381, 882, 383 
Report of a Case of Tabes, with Especial Refereuce to the Changes in 
the Posterior Root Ganglia. Figs. 1-6 ... ... 392, 396, 397, 398 

Preliminary Observations on the Etiology of Asylum Dysentery. 

Figs. 1,2 ... ... ... ... ... 405,415 

Three Cases of Tumour of the Third Ventricle. Figs. 1-8 421, 422, 424, 425 

428, 429, 430, 439 

A Telangiectasis of the left Frontal Lobe, with Epileptiform Convulsions. 

Plates VI., VII. Figs. 1 3 ... ... ... 445, 447, 448, 450 

Three Dissimilar Cases of Multiple Lesions of the Central Nervous 
System. Figs. 1-8. Diagrams I.-III. 459, 462, 464, 467, 474, 479, 481, 

483, 487 

Preliminary Communication upon the Changes in the Brain, Spinal 
Cord, Muscles and other Organs found in Persons Dying after Pro¬ 
longed Epileptiform Convulsions. Plates VIII., IX. Figs. 1-4 

500, 503, 504, 505, 50G 

Alcoholic Atrophy in the Central and Peripheral Nervous System of a 
Woman. Plate X. ... ... . ... ... ... 520 

Observations on the Normal Anatomy of the 9th, 10th, 11th and 12th 
Cranial Nerves. Figs. 1-3 ... ... ... 545, 546, 547, 548, 549 


BY Dr. W. J. COLLINS, M.S., B.Sc., F.R.C.S. 

Late Chairman London County Council. 

In now presenting to the London County Council, the 
Profession and the Public the first fruits of the researches 
carried on at Claybury Laboratory under the superinten¬ 
dence of Dr. F. W. Mott, F.R.S., it has been thought fit 
to preface these Archives, which it is hoped will annually 
enlarge our knowledge of the pathology of mental diseases, 
by a brief account of the origin, objects and equipment of 
the County Asylums Laboratory. 

Various momenta have contributed to the recognition 
of the need of more determined, systematic, and exhaustive 
research into the causes of Insanity. The mere increase of 
its prevalence, annually asserted by official statistics, must 
alone arrest the thoughtful attention of the ratepayer no 
less than of the sanitarian. 

The pathologist regarding the whole of medicine as but 
applied physiology, having, by modern methods of research, 
achieved so much and having revolutionised treatment in so 
many of the diseases which afflict the body, inspired thereby, 
has been attracted, by the very complexity and magnitude of 
the task, to endeavour by similar means to annex this dark 
and out-lying continent of pathology to the better known, 
more illumined and well-worn tracks of medical science. 

The reasons for this relatively backward state of the 
Pathology of Insanity, compared with the well-cultivated 
fields of other areas of disease, are not far to seek. Among 
these are—the complexity alike of chemical constitution and 
physical structure of the nervous system of man; the 
proportionate littleness of the lesion with the magnitude 
of the malady; inacessibility to direct investigation, further 
obscured by the complaint itself frequently precluding the 
sufferer from accurately complaining. To these inherent 



difficulties there have been in the past extrinsic difficulties 
super-added; an element of mystery has .been interwoven 
with mental alienation and in the form of witchcraft or 
demonology or electro-biology or spurious spiritualism 
has often sufficed to check, encumber, or distort efforts 
after a true Pathology of the Mind. 

The change of objective, too, in dealing with the insane 
in harmony with “ the new philanthropy” which, for the 
last hundred years, has ameliorated the lot of the poor, 
the criminal, the outcast and the sick, has had its influence 
in bringing modem science as well as tender kindness to 
the succour of the mentally afflicted. Asylums and hospitals 
originally contrived for the removal of the demoniac and the 
offensive from the public gaze, have now become, under the 
reforming influence of philanthropic zeal, palatial in accom¬ 
modation, humane in their administration, and last, though 
not least, agencies for obtaining fresh knowledge for the 
alleviation and prevention of those social banes whose 
neglect first inspired the establishment of “ bedlams ” and 

Hogarth, who died in 1764, has recorded on canvas the 
scenes of squalor and cruelty which these Bethlehems of the 
last century concealed within their walls. What a study 
in pathological portraiture is that scene in Bedlam in the 
Rake’s progress. There we behold on one small canvas the 
crowded panorama of London’s intellectual refuse; there 
sits apart the large-brained melancholy with clasped hands, 
listless and unaffected by the barking dog; above him the 
general paralytic, self-donned with dunce’s cap and tawdry 
sceptre in hand, is dilating of his wealth and power. The 
solitary cell to the left shows, stretched on straw, the last 
stage of senile dementia; in the fore-front, the manacles 
are being applied to the limbs of the maniac, whose head 
is undergoing examination by the apothecary, as if in 
dubious anticipation of our modern methods of cerebral 
localisation. The final satiric touch is given by the visit of 
two ladies of quality and fashion, inspired by prurient 
curiosity ; and perhaps the one redeeming feature of the 
whole is the mob-capped nurse, whose ministrations serve 



as an earnest of that great reform in the care of the sick 
and insane which it has been the privilege of our era to 
have witnessed. 

Since Hogarth’s time, Pinel in Paris, Conolly of 
Hanwell, and Tuke at York, have, by their initiative, 
effected a revolution in the treatment of the insane. It has 
remained for the present generation to add investigation 
by the recognised methods of science, as a needed auxiliary 
for prevention and cure, to the amelioration already effected 
by philanthropic zeal and competent administration. 

When the London County Council took over the charge 
of the lunacy of London from the Justices it was soon 
recognised that there was room for improvement in the 
matter of pathological investigation and research. It was 
felt that the Council, as the lunacy authority for London, 
should not only be on a level with provincial and continental 
towns, but that the occasion was opportune for establishing 
a central laboratory replete with all the most modern 
equipments for the study of psychological medicine in its 
widest sense. Accordingly, at the end of 1892, it was 
referred to a committee to consider the propriety of 
appointing a pathologist to the London County Asylums, 
the nature of the duties of such office, and the manner in 
which provision should be made for their performance. 

Information gathered from the medical superintendents 
of our asylums, from the provinces and from abroad, showed 
. conclusively that less was being accomplished in the matter 
of pathological research into the causes of insanity in 
London than opportunity and necessity alike demanded. 
Post-mortem examinations were, indeed, being extensively 
made, but they had for their object rather the requirements 
of routine administration than the enlargement of our 
sphere of knowledge. The observation implies no reflection 
on the asylums’ staffs. Their energies were fully absorbed 
in clinical and administrative work, and while the 
material for pathological research in its very amplitude 
constituted a bar to exhaustive investigation, the provision 
for such investigation was neither adequate nor modem. 

As the result of the report of the Special Committee, 



the Council approved the establishment of a laboratory at 
an estimated cost of £4,000, the provision of fittings and 
apparatus at a cost of £800, and the appointment of a 
pathologist at £700 per annum. 

The Committee, firmly convinced that investigation 
likely to be eventually of service to those who are committed 
to our care must combine clinical with pathological 
research, obtained the Council’s approval to locating the 
laboratory at the first asylum built by the London 
County Council, namely, Claybury, which was then in 
course of completion. 

Dr. F. W. Mott, M.D. (Lond.), F.R.S., having been 
appointed pathologist to the County Asylums and Director of 
the laboratory, was at first engaged in purchasing and 
fitting up apparatus, after a visit to many of the best 
equipped laboratories in France and Germany had familiar¬ 
ised him with the latest and most approved developments 
of modern neuro-pathology. 

The laboratory, designed by Mr. Hine, is built apart 
from the main structure of the asylum and is self-con¬ 
tained. It is composed of two portions, connected by a 
covered way. The larger front portion contains (1) a 
Physical Research room containing an ophthalmoscope, 
fitted with a special electric lamp, laryngoscope, batteries, 
and other apparatus for clinical investigation; (2) a 

Chemical and Bacteriological department with reagents, 
balance, gas, water, air-pump, and a draught cupboard ; 
(3) a Histological department at the rear of the last named 
with a good northern light and benches with microtomes, 
microscopes and staining fluids, arranged for several 
workers; (4) a Photographic studio with dark chamber 

and electrically fitted photomicrographic apparatus, and 
a screen for the purpose of demonstrations. A spacious 
central Museum and Library connects these four depart¬ 
ments, and a room for the Director completes this portion 
of the building. 

Across the covered way is the Post-Mortem room, well 
fitted and well lit; adjacent to it is the curator’s room, for 
the preparation of specimens. Separate male and female 



mortuaries, cool and of good dimensions, to which friends 
are admitted to view the deceased, intervene between the 
post-mortem department and a convenient waiting room. 
The construction and working of the laboratory has been 
contrived with a view to secure that sentiment shall be 
respected and sanitation satisfied. Perhaps it is well to add 
that the building is not licensed for vivisection, and no 
such practice will be allowed therein. At Dr. Mott’s 
suggestion, and with the assistance of Mr. Clifford Smith, 
a valuable addition has been made to the laboratory in 
the shape of a cold chamber, whereby decomposition is 
prevented, thus enabling microscopic examination of tissues 
to be rendered independent of the complicating results of 
such process. This, as well as the whole arrangement of 
the laboratory, received the highest eulogium from Pro¬ 
fessor Yirchow, the Citizen Pathologist of Berlin, on his 
recent visit to this country. 

We thus see that there are now provided under the 
London County Council at Claybury means and methods 
for applying persistent interrogatories to what has hitherto 
been justly regarded as the most obscure, mysterious and 
sphinx-like region of disease. A visit any day to the 
laboratory will show that while those competent for such 
research are naturally few, they are not unfit. The 
Technical Education Board has bestowed research scholar¬ 
ships, tenable at the laboratory, upon Dr. Wakelin Barratt, 
B.S., B.Sc. Lond., Mrs. Williams and Mr. Tredgold. 
Dr. Head, F.R.S., Dr. Hamilton Wright, Mr. Durham, 
Mr. Salaman and Mr. Howard Green, have, under Dr. 
Mott’s guidance, carried on elaborate researches while some 
of the assistant officers of the asylums have, as was hoped 
by the promoters, associated themselves with Dr. Mott in 
the clinico-pathological study of various mental diseases. 
It cannot be too widely known that all earnest workers in 
the Pathology of Insanity are welcome at Claybury, and 
the advantages offered by the laboratory are freely placed 
at their disposal. 

A survey of the papers now published will convince the 
reader that a wide view of the scope of the work in hand 



has impressed itself upon all concerned, and all available 
means of investigation have been laid under contribution. 
Research is held to be something more than mere micro- 
scopising and test-tubing. The anatomo-pathological 
method of Charcot, which enabled him to extract brilliant 
results from the mental and moral dust-bin of Salpetriere, 
is being pressed into fresh directions. Statistical, historical, 
racial, and geographical considerations enter into the ken 
of the pathologist as much as into that of the psychologist; 
and sociology, that newest of the sciences, has, it will be 
seen, a very proximate relation to the matter in hand. It 
is to General Paralysis that the greatest amount of attention 
has, in the past year, been directed. The potent influence 
of syphilis is abundantly brought out, though it remains 
doubtful whether this is excited by way of specific infection 
or as an added influence to that excess in Baccho et Venere 
which eventuates in neurasthenia. It also appears that 
General Paralysis must take its place with other organic 
degenerations of the nervous system, differing from such 
as Tabes and others, rather in the area of distribution of 
the degeneration than in its essential nature. 

These and many other suggestions will occur to the 
student of the following pages which, as the first fruits 
of work done at the Claybury Laboratory, may, it is 
hoped, usher in an era of accelerated progress in the 
scientific unravelling of the maze of mental pathology. 






The study of the etiology and pathology of insanity is 
beset with many difficulties, especially when the subjects of 
investigation are derived from the lower and more ignorant 
classes. Direct inquiries into their family history or their 
previous illnesses are too often attended with barren or 
uncertain results. Such patients cannot tell you many 
reliable facts—either they have no friends, or, should they 
be visited, such friends are unable to give any definite 

The difficulties, however, do not so much arise here as 
in the mode in which the patient is transferred from his 
home to the infirmary, and from the infirmary to the 
asylum; so that when he reaches the latter institution often 
but little is known of the course the symptoms have taken 
since the onset of his illness. The information which is 
afforded to the authorities is merely the certificate of in¬ 
sanity—enough certainly for administrative purposes, but 
not for scientific inquiry. Again, the notes which are taken 
in the asylums and the mode of classification of patients 



may be admirable enough for the administration of such a 
large number of patients, but are not adapted for service to 
a scientific inquirer; and this must be so, while the present 
system exists. 

The scheme now under consideration of admission of all 
patients first into Receiving Houses would, I feel convinced, 
aid much in preventing many of the present disabilities, 
and tend to promote the prevention and cure of some forms 
of insanity. 

The question also naturally arises whether it would be 
more economical to modify the present system by having a 
larger number of medical officers, a plan now finding favour 
in America, but long since adopted in Germany. 

Our present system of inquiry by means of a printed 
form sent to the friends to fill up, on which is stated that 
it is not compulsory to reply, but that treatment would be 
assisted thereby, is practically useless. I have found out 
myself, by careful inquiry from the relatives of deceased 
patients, most important facts relating to the causation of 
the disease which have not appeared in the notes; and such 
information has always been readily given to me to the 
best of their ability. 

In England statistics must always be more or less fal¬ 
lacious in regard to certain questions; for example, the 
relation of syphilis to various diseases. Especially is this 
fallacy likely to occur in London, where there are so many 
special hospitals. A man may be infected, he attends the 
Lock Hospital; after a certain time, perhaps in the secon¬ 
dary stage of the disease, he gets a squint, and turns up at 
an eye hospital; or if he has a paralysis, he attends a general 
hospital, or one for nervous diseases; or he may become 
incapacitated mentally or physically, and be transferred to 
the workhouse infirmary, and possibly afterwards to an 
asylum. His antecedents are often not known, and he is 
either unwilling or incapable of giving any reliable infor¬ 
mation. It will thus be seen that the number of cases of 
brain disease which are seen at the Lock Hospital affords 
no indication of the number of cases of syphilis with nervous 


Abroad, the system of administering .relief in one general 
hospital affords the opportunity for obtaining reliable 
statistics, and it is from such information obtained from 
such sources that a great many important facts relating to 
the influence of syphilis in the production of diseases of the 
nervous system have been collected. 

My hospital experience had led me to believe that syphilis 
is by far the most important cause of organic brain disease 
in adults, and a history of syphilis was obtainable in the 
majority of cases of locomotor ataxy; moreover, it is the 
general practice of hospital physicians, even where no 
history of infection can he obtained, to try anti-syphilitic 
remedies in certain cases of organic brain disease, and this 
often with the most satisfactory results. I have found that 
about 20 per cent, to 25 per cent, of the male adults attend¬ 
ing my out-patient department for various diseases had 
been certainly infected. A much larger number had suffered 
from some form of venereal disease. It is calculated that 
about 1 per cent, to 2 per cent, of persons infected suffer 
with brain syphilis exclusive of para-syphilitic affections ; 
and Fournier maintains that nervous disease is the com¬ 
monest complication of tertiary syphilis. I was therefore 
surprised to find in the statistics and reports of the London 
County Asylums little or no mention made of syphilis as a 
cause of insanity. I was all the more surprised when I 
read the statistics of foreign asylums, especially those of 
Germany, Austria, and Scandinavia, and I attributed the 
difference to the difficulties in obtaining reliable information 
in England. 

I have, however, seen the most obvious syphilitic residua 
overlooked in the notes of cases in the asylums; the routine 
colour of the hair, the appearance of the tongue, the shape 
of the palate and the religion of the patient are put down, 
but even such coarse objective symptoms as hemiplegia and 
facial paralysis have occasionally not been recorded in the 

If a comparison be made between the number of new 
cases attributable to syphilis in the reports of 1897 and 1898 
at Claybury, it may be gathered that in the latter year more 



attention had been devoted to the subject, for oat of a total 
of 958 patients admitted daring 1896 in three the probable 
cause of insanity is noted to be venereal disease, while out 
of a total of 678 admitted in 1897 it is forty. 

We have only to refer to the paper of Mr. H. W. Lewis 
on “ General Paralysis ” (p. 223) to note the effect in numbers 
upon the relation of syphilis to general paralysis, which a 
careful inquiry and investigation can make. 

Dr. Jones, at a recent meeting of the Medico-Psycho¬ 
logical Society, stated that he slowly, but nevertheless 
surely, is being convinced that syphilis plays a most im¬ 
portant part in the production of general paralysis. And I 
had a letter from Dr. Wigglesworth about this disease, 
stating that more careful inquiry into the history of the 
patients showed that syphilis was more frequently asso¬ 
ciated with general paralysis than he had previously 
believed. I shall endeavour to show in the two following 
papers that syphilis is one of the most important extrinsic 
factors in the production of insanity and that it may operate 
in two ways from a pathological standpoint. 

Firstly , the poison may produce a specific inflammatory 
process affecting the membranes and blood-vessels of the 
central nervous system, either of which may be affected 
separately or together. The process may be local or general. 
The inflammatory process may produce direct irritation or 
destruction of the nervous elements, the blood-vessels may 
be partially • or completely occluded and the effects on 
function will depend on the extent of the process. The 
inflammatory process may also give rise to neoplastic 
growths, which may undergo regressive metamorphosis in 
the older parts (gummata), but all the processes are patho¬ 
logically identical, and it may be observed that there is 
really no absolute specific character about them, yet ex¬ 
perience has taught us that the lesions are pathognomic of 
syphilis. Until the tubercle bacillus was discovered it would 
have been difficult to have distinguished some syphilitic 
lesions from tuberculous lesions. When the bacillus of 
Lustgarten was discovered it was hoped that the specific 
organism of syphilis had been found, but subsequent obser- 


vations have shown that syphilis, like many other contagious 
and infectious diseases, may be assumed only on the slander 
basis of analogy to be due to a living organism. 

Secondly, syphilis whether acquired or inherited, may 
lower the specific vital energy of the component cells-of the 
body as a whole, or the cells of particular tissues or organs. 
Fournier, the greatest authority on this disease, terms these 
affections parasyphilitic. He points out that in hereditary 
syphilis you may have a general or partial dystrophy, pro¬ 
ducing organic malformations, notably of the teeth; arrest 
or delay in development, physical and intellectual, infantilism, 
stunted growth to such a degree as to produce dwarfs (Fr. 
Nanism), cachexia, and such a deficiency of vitality that 
death may occhr without any obvious cause, none even found 
at the autopsy; it may also affect the development of the 
bones causing rickets and cranio-tabes. None of these lesions 
are truly specific, but in a great many cases syphilis is the 
cause. In fact, the malformations of the teeth are almost 
pathognomic of the disease. 

Fournier classifies the parasyphilitic diseases of the 
nervous system as follows :—(1) acute hystero-neurasthenia 
of the secondary period; (2) hystero-syphilis; (3) tabes 
dorsalis; (4) general paralysis of the insane; (5) a special 
form of epiplepsy ; (6) a special form of muscular atrophy. 

Nos. 3, 4 and 5, together with congenital imbecility and 
idiocy, may be considered as the parasyphilitic affections of 
the inherited form of the disease; but before passing on to 
a fuller consideration of the subject, it is necessary to men¬ 
tion here the important part that syphilis plays in the pro¬ 
duction of endarteritis deformans and obliterating arterio¬ 
sclerosis, causing secondary degenerations and softening. 

Thus, seeing that syphilis is the most prevalent, the 
most persistent and one of the most powerful poisons acting 
upon the human body in manifold ways, it is surprising that 
so little attention has been paid by the authorities in the 
asylums to eliciting a careful history and making good 
observations for the residua of syphilis, especially when it is 
remembered that the true syphilitic diseases of the nervous 
system are amenable to treatment in the early stages. It 



is, however, no argument against syphilis being the cause of 
those affections which are termed parasyphilitic to say that 
because iodide of potassium and mercury do no good the 
diseases are therefore not of syphilitic origin, because we 
might as well expect by giving such drugs to be able to give 
new teeth or to convert a dwarf into a full-sized man. In 
a normal healthy organism all the primitive nerve-cells, 
termed neuroblasts—out of which the whole of the complex 
neurons which make up the. nervous system are to be 
developed—are present at birth, the growth and develop¬ 
ment of the nervous system being due to increasing com¬ 
plexity of structure and not to increase of numbers; 1 and 
inasmuch as regeneration of the nerve-cells does not take 
place, it may be presumed that the neurons are perpetual 
elements, capable of molecular but not of organic change, 
endowed in the healthy animal with a specific energy 
calculated to last as long as the organism. Should a poison 
enter the system, such as the syphilitic virus, it may so 
lower the vitality that under the influence of stress prema¬ 
ture decay occurs, and I think this argument is borne out 
in a striking manner when consideration is given to the 
history of the cases of juvenile general paralysis which I 
have collected. In nearly all of these cases the signs or 
a history of inherited syphilis are plainly shown. 

Although the relation of syphilis to insanity is a matter 
of dispute in this country, all authorities are agreed that 
alcoholic excesses are among the most important preventible 
causes of insanity. It will be shown that the evil effects of 
syphilis are greatly aggravated and often directly determined 
by abuse of alcohol. Excesses in baccho et venere frequently 
go together. F. W. Mott. 

1 Schulz found that the same number of nerve-fibres in the optic nerve 
exist in an animal at birth as in an adult, the only difference oeing the 

Pakt I. 



Pathologist to the London County Asylums , and Physician in Charge of Out- 
Patients , Charing Cross Hospital. 

Literature shows that Morgagni in his “De Sedibus 
Morborum” described syphilitic disease of the brain, but, 
owing to the teaching of John Hunter that visceral lesions 
did not follow syphilitic infection, brain syphilis was not 
believed for a long time to exist. Isolated observations, 
however, began to be made by Lallemand, Rayer, Dittrich 
and others about fifty years ago, and then Virchow’s 
teaching placed the disease upon a sure basis, with the 
result that numerous observers abroad and in our own 
country published cases of undoubted brain syphilis. Wilks, 
Bristowe and Clifford Allbutt contributed their experiences, 
and it was the latter who in 1870 first described the micro¬ 
scopic character of syphilitic disease of the cerebral arteries. 
Four years later Heubner, in a classical monograph, at once 
important and practical, established the relation which 
syphilis bears to diseases of the nervous system by the 
effect of the poison upon the cerebral arteries. Barlow 
showed that the same pathological conditions obtain in the 
hereditary as in the acquired form of the disease. The 
important contributions made by Wunderlich, Jackson, 
Erb, Oppenheim, Gowers, Lang, Hutchinson, Mickle and 
others have all tended to show the important part played by 
syphilis in the production of organic brain disease. Fournier 
was the first, however, to express the view that locomotor 
ataxy (tabes) is of syphilitic origin, and found strong support 



in the collected statistics of Erb and Gowers; subsequently, 
he applied the same view to general paralysis. Now daily in 
all countries fresh evidence is being collected in support of 
this very important doctrine that these two degenerative 
processes of the nervous system are of syphilitic origin. 

It was generally accepted, and is still by many authori¬ 
ties, that syphilitic nervous diseases occur especially in the 
later tertiary periods. Fournier himself stated in his first 
edition that syphilitic nervous disease seldom occurs in the 
first or second year after infection. Heubner states that 
almost without exception a year elapses before nervous 
affections occur; generally more than three years elapse. 
He also considered that several years, usually many years, 
intervene between infection and the onset of syphilitic 
gummata or disease of the vessels. This is not my ex¬ 
perience, as the cases which I record will show; there is 
practically no period after infection at which syphilitic brain 
disease may not occur, but the most intractable to treat¬ 
ment, the most severe and generalised forms of the disease, 
are those which occurred within the first two or three years. 
One of the first observers to doubt the older view was Bumpf, 
who collected statistics of thirteen cases. Charles Mauriae, 
also, made the important observation that cerebro-spinal 
syphilis occurred most frequently in the first year. Lang 
refers to a collection of a hundred cases made by Braus 
in 1892, of which the history of infection was obtainable 
and nearly half of which occurred within the first year. 
Naunyn analysed forty-five of his own cases and 290 collected 
cases, and he came to the conclusion that syphilitic diseases 
of the nervous system appear more frequently in the first 
year after infection and that their frequency diminishes 
from year to year. With regard to the evidence adduced 
from collected cases, there is a fallacy, viz., that early and 
severe cases would be looked upon as cases of interest, and 
more likely, therefore, to be published than others. 

In forty cases of cerebral syphilis which have come 
under my observation in which a history of syphilis and the 
time which has elapsed between the onset of the cerebral 
symptoms and the existence of the primary sore has been 


determined, it was found that four occurred in the first 
year, seven in the second year, six in the third year and 
three in the fourth year, and the remainder at subsequent 
periods. These were mostly hospital cases, for, as a rule, 
asylum cases do not afford the necessary information unless 
they have been treated at a hospital before they were 
demented and the notes taken there are obtainable. Lang 
has pointed out that often during the outbreak of the 
syphilitic exanthem, headache, giddiness, pyrexia, increased 
frequency of the pulse rate or slowness of the same, and 
inequality of the pupils sometimes occur, probably due to 
meningeal irritation (vide Case 10). 

Enquiry of two of my colleagues, Mr. Bloxam and Mr. 
Gibbs, surgeons at the Lock Hospital, leads me to believe 
that this is a rare condition. Many of the older writers— 
Leon Gros, Lancereaux, Zambaco, Llungren and others— 
have described cases of early syphilitic disease of the nervous 
system and Kahler has described a case which occurred 
while the primary sore was yet unhealed, also a patient 
of Nonne was affected within three months of infection, 
and a case has been described by Gilles de la Tourette 
and Hudelo that occurred within four weeks of infection. 
The earliest in my cases was about six months, and of these 
there were probably four (vide Cases 10, 13, 31, 39), and it 
is possible that symptoms in two cases were present before 
they came under medical observation. Gower’s experience 
is that one-fourth of the cases occur within the first two 
years after infection. 

Again, Beaudoin has collected twenty-six cases in 
Fournier’s clinic, in which nervous symptoms occurred 
within three to six months after infection. I have found 
from statements made to me by surgeons at the Lock 
Hospital that they very seldom see cases presenting nervous 
symptoms soon after infection, and this I attribute partly 
to the fact that as soon as they get eye symptoms, headache 
and vomiting, paralysis, mental affection, or other such 
symptoms, they come under treatment in special hospitals, 
general hospitals, workhouse infirmaries or asylums (vide 
Case 31). 



The question whether mild or severe forms of syphilitic 
infection are more liable to be followed by severe diseases of 
the nervous system is one of considerable importance, and 
has been discussed by many authorities. Sir William 
Broadbent was one of the first to draw attention to the fact 
that severe nervous symptoms often follow mild attacks. 
Gilbert and Lion consider that spinal syphilis in opposition 
to brain syphilis comes from the severe forms of the disease. 
Hjellman comes to the conclusion that severe forms of 
brain syphilis arise from the mild and moderately severe 
forms of infection. My experience seems to show that all 
forms of syphilis may be followed by severe nervous 
symptoms, that the mild forms are probably prone to be 
followed by serious disease, because either they have been 
looked upon as simple soft sores or have been only very 
inadequately treated—the fault sometimes resting with the 
patient, but as often as not with the doctor. It seems, 
however, to be a fact that the mild forms of syphilis are 
particularly prone to be followed by the parasyphilitic 
affections, tabes and general paralysis, and Hitzig has 
formulated a theory that there are several poisons in 
venereal infection and that the soft sore is an infection with 
a poison that is especially injurious to the vitality of the 
nervous system. There is an analogy in diphtheria, the 
mild cases of which are more often followed by paralysis; 
in fact, I have frequently diagnosed previous diphtheritic 
infection by the paralytic symptoms which followed, and on 
inquiry one finds the patient did have a sore throat, which 
gave but little trouble. Dr. Ferrier, at the British Association 
at Edinburgh, 1898, stated that his experience led him to 
associate tabes and general paralysis with syphilis to such 
an extent that he assumed that a man suffering with either 
of these diseases had been infected. 

It is often presumed that the soft sore cannot be 
syphilis; this is an error and often leads to inefficient 
treatment. Many severe cases of cerebral syphilis I have 
found to follow a so-called soft sore; moreover, it is thought 
that if a patient has had a bubo therefore he cannot have 
had syphilis; this is also an error, for I have seen many 


cases of what was called soft sore (which had been treated 
only for a few weeks locally) followed sometimes by mild 
secondary symptoms end in serious nervous disease. Some¬ 
times a urethral chancre is overlooked and the patient is 
thought to be suffering with gonorrhoea {vide Case 26). 

Most of the leading authorities hold the opinion that 
brain syphilis is much less likely to follow when the disease 
has been efficiently treated with mercury and iodide of 

The history of most oi my cases showed that the patients 
had been treated in an inefficient or insufficient manner after 
infection; there are, however, one or two notable exceptions 
C vide Cases 10, 31, and 30). 

Hjellmann has made accurate observations upon this 
subject, and he has found that 82 per cent, to 85 per cent, 
of brain syphilis were those in which only an imperfect 
treatment had been carried out. 

Injuries to the head have long been recognised as a 
cause of the setting up of syphilitic brain disease, for just as 
a kick on the shin will produce a node, so a blow on the 
head will set up a gummatous meningitis which may remain 
local or be the starting-point of an extending disease {vide 
Cases 7 and 8). 

Of all the causes which predispose to syphilitic brain 
disease alcoholic excess is the most important {vide numerous 
cases recorded), but excesses of any kind, especially in 
baccho et venere, or mental stress, tend to develop the 
disease; lead poisoning may he a factor {vide Case 49). 

Certain individuals are more prone to affection of the 
nervous system than others, owing to an inherited neuro¬ 
pathic tendency; it is strange that two brothers should 
have been affected by very similar symptoms almost at the 
same time or within a year of the same age {vide Cases 16 
and 17). 

Gilles de. la Tourette has recorded a series of nervous 
cases following infection from the same source. 

It is said that one-fourth of the cases of brain syphilis 
recover, another fourth improve decidedly, at least one-half 
die or only partially recover and remain mentally or physi- 



cally incapacitated. Very much depends on early and 
effectual treatment; it is, therefore, of special importance 
to emphasise the fact that cerebral syphilis seldom strikes 
without warning symptoms; too often the warning is 
neglected, not only by the patient, but by the medical man, 
or more frequently this occurs when the poison acts first 
upon “ silent parts of the brain,” producing mental symp¬ 
toms only. It is fortunate that ocular paralysis is so 
frequent, for this attracts the patient’s attention and takes 
him usually to the eye hospital, where the nature of the 
disease is recognised and appropriate treatment given. 

It is usual to consider syphilitic brain disease under the 
following headings:—Basic meningitis, meningitis of the 
convexity, cerebro-spinal meningitis, arteritis and neoplastic 
formations (gummata), encephalitis. 

One finds usually all these conditions combined in the 
severe and early forms of the disease. At least, that is my 
experience, as shown by the recorded cases in which autopsies 
were performed. 

Basic Syphilitic Meningitis. 

The cases which have come under my observation show 
that the base of the brain is the most frequent seat in which 
the disease commences. Especially is it liable to begin about 
the optic chiasma. In nearly all the fatal cases which I 
have examined {vide Cases 33 to 45) there has been gum¬ 
matous meningitis about the base. All of these have been 
associated with some degree of spinal meningitis, but in 
only one were symptoms of spinal affection noted during 
life. All these cases also showed a profound affection of the 
coats of the arteries, great and small, and in five cases 
gummatous masses existed in the brain. The process, in 
fact, seems to start where the cerebro-spinal fluid is most 
abundant and to spread up the Sylvian fissures, forming 
there gummatous masses, and to extend thence along the 
perivascular lymphatics into the brain substance—in one case 
producing little nodular swellings in the lateral ventricles, 
ependymal gummata {vide photograph, p. 116). All the cases 
associated with gummata had severe mental symptoms and 


bore such resemblance to general paralysis that they were 
usually diagnosed by the medical officers in the asylums as 


Headache is one of the commonest, one of the earliest, 
and one of the most constant symptoms; sometimes it 
precedes all other symptoms by months or even years; it is 
not unfrequently associated with vomiting of a cerebral 
character. This last symptom may, however, be absent 
during the whole course of the disease. In other cases, 
according to Oppenheim, headache and vomiting>may he the 
sole manifestation of the disease for months or even for 
years. There are very few of the cases here recorded of 
syphilitic meningitis in which headache was absent during 
the whole course of the disease. 

The pain is paroxysmal; when it reaches its greatest 
intensity it may be stabbing, boring and excruciating, but 
this may gradually die down, leaving only a dull aching. 
It is curious but very characteristic that the pain should be 
most severe at night or in the early morning; it may even 
awake the patient at a regular time. In the basic form of 
the disease the pain is referred to the frontal, parietal and 
temporal regions and is deep-seated and cannot be definitely 
localised; it may later on spread to the occipital region, 
the neck and the spine ; sometimes pain is referred to the 
back of the eye. In this form of the disease the pain is not 
usually influenced by pressure and there is no definite local 
tenderness, the same as when the convexity is affected. 

Stiffness of the neck may be complained of, and the 
nocturnal pain generally prevents sleep, and this insomnia 
no doubt aggravates the affection of the nervous system. 
The patient is subject to attacks of vertigo , reeling, staggering 
and loss of balance. 

Temperature .—There is great variability, not only in the 
opinion of authors as to existence of pyrexia or not, but in 
the temperature itself, according to the form of the disease. 
It is, however, pretty generally recognised that syphilitic 
meningitis differs from other forms of meningitis, e.g., 



tubercular, by the absence of pyrexia. Heubner, however, 
states that very high fever may occur. I have myself seen 
this happen when there have been prolonged convulsions. 
The temperature is usually normal, however, or even sub¬ 
normal (vide Cases 5,10, 35,44, &c.). If pyrexia be present, 
it is usually of an anomalous form ; it may be remittent, and 
sometimes at the onset of the disease there may be a rise of 
temperature in the evening, but in my experience pyrexia 
is quite unusual in syphilitic brain disease. 

Ocular affections. —Of all the symptoms of syphilitic 
basilar meningitis affections of the optic chiasma and 
nerves and of the nerves supplying the muscles of the eyeball 
are the most frequent and important. This we should 
expect, for, as already stated, the interpeduncular space is 
the most common and earliest seat of the inflammatory pro¬ 
cess ; it is only natural, therefore, to expect that these 
nerves are especially prone to be affected. The observations 
of early authors on brain syphilis showed how frequent 
affections of the optic nerve and the nerves supplying the 
muscles of the eye occur. Yon Graefe in 160 cases found 
that in more than half there was some form of oculo-motor 
paralysis. Alexander found that in 72 per cent, there was 
unilateral paralysis of the oculo-motor nerve, and both 
Ricord and Fournier designate this ophthalmoplegia “ la 
signature de la verole.” Uhtoff concludes from his observa¬ 
tions that in only about 15 per cent, of all cases of cerebral 
syphilis are eye disturbances of some form or another absent. 
Oppenheim in fourteen out of seventeen cases in which an 
autopsy was made found affection of the optic nerve and 
optic tract. In the asylum cases which have come under 
my observation, it was very seldom that an ophthalmoscopic 
examination was made. In a number of the cases there 
must have been affection of the optic nerves and tracts from 
the observations made post mortem, for they showed that 
these structures were more or less affected seriously by the 
gummatous meningitis. Optic neuritis was noted in ten of 
the cases; probably this does not represent the proportion 
affected. On the other hand, such a severe case as 35 
showed no neuritis while in the London Hospital, but post 


mortem there was well-marked optic neuritis. Nor could I 
find any in 30 and 31. Some of the cases sent to the 
hospital showed changes in the fundus, e.g., 5, 11, 12,16,17. 

Brain syphilis may be accompanied by the following 
ophthalmoscopic changes:—(1) Choked disc, due to intra¬ 
cranial pressure; (2) optic neuritis; (3) neuritic atrophy; 
(4) simple atrophic degenerations. 

Choked disc when present almost always affects both 
eyes, whilst neuritis may remain limited to one eye. 
Generally speaking, there is a considerable difference in the 
intensity of the affection between the two eyes. Optic 
neuritis as a sole and uncomplicated manifestation of basal 
syphilis is extremely rare. 

Oppenheim speaks of hemianopsy as being frequent. I 
have met with one case in my hospital practice which I 
believed to be of syphilitic origin. It was in a man who 
was sent to me by Mr. Treacher Collins : he had loss of the 
left half of the field of vision ; the nasal side of the retina did 
not respond to light on the left side, whereas the temporal 
side did—Wernicke’s pupil reaction; it must therefore have 
been a lesion of the right optic tract. 

In Case R.A.M., the patient must have had some degree of 
hemianopsy or impairment of the field of vision without Wer¬ 
nicke’s pupil phenomenon, for there was found post mortem 
a gumma in the occipital lobe of the left side; but she was 
too demented to give any reliable answers even had she been 
tested. It is remarkable that for a long time impaired vision 
may occur with a normal fundus; this especially applies to 

Gowers states that syphilitic disease of the arteries by 
itself never causes optic neuritis, and Uhtoflf, with his large 
experience, supports this statement, although various authors 
have described changes in the arterial walls with narrowing 
of the lumen. I examined the optic nerves in three of the 
cases in which there was universal endarteritis cerebri; but 
I observed no narrowing of the lumen of the arteries micro¬ 
scopically, nor could I find any changes in the arteries in 
three cases of primary atrophy. I have met with chorio¬ 
retinitis in four cases of general paralysis, two of the juvenile 



form, also in a case of congenital hemiplegia and epilepsy, 
Case 29, and in one case of syphilitic brain disease, viz., 38. 
It is impossible to take the field of vision in asylum cases as 
a rule. In one of my hospital cases, 12, concentric limita¬ 
tion of the field of vision was found by Mr. Treacher Collins. 
Uhtoff states that it occurred in 5 per cent, of his cases; 
there may be choked disc in syphilitic meningitis, but as the 
disease subsides* the disc may return to the normal ( vide Cases 
12, 11, 17). Of all the cranial nerves the oculo-niotor 
nerve is by far the most frequently affected; it may be 
affected on one side or on both sides, completely or par¬ 
tially ; as a rule, all the muscles supplied by the third nerve 
are not paralysed. The muscle especially liable to be para¬ 
lysed, and the earliest also, is the levator palpebrse, causing 
ptosis,—this condition should always make one think of 
syphilis. Sometimes the pupil only is affected, frequently 
it is dilated on one side and fixed to light and accommoda¬ 
tion ; sometimes only the light reflex is lost. I have seen a 
case in which both oculo-motor nerves were completely 
paralysed; it was sent to me by Mr. Treacher Collins. A 
woman, aged 51, who had, besides paresis in the limbs, 
ankle clonus and exaggerated knee-jerks, complete bilateral 
ophthalmoplegia externa and interna, and when first seen 
she was in a stupid dazed condition. Six weeks’ treatment 
with large doses of iodide of potassium led to an almost 
perfect recovery. Oppenheim states that in seventeen cases 
upon which autopsies were made, the oculo-motor nerves 
were affected ten times ; in six cases bilaterally; in 100 
cases observed clinically it was affected thirty-four times. 
The sixth nerve was affected in 16 per cent., and the fourth 
nerve in 5 per cent. Among my cases the oculo-motor was 
affected in eighteen cases, about the same proportion. The 
abducens was noted as twice affected in my cases, and the 
fourth not at all. The fifth nerve is nearly always affected 
unilaterally, though rare cases have been described in which 
both nerves have been affected ( vide Case 15). 

The sensory trunk is more liable to be affected than the 
motor ; in the case referred to there was also the rare con¬ 
dition of enophthalmos. 


As a rale, the patient complains of severe pains over the 
distribution of the nerves hypersesthesia; hypaesthesia, or 
even complete anaesthesia may exist in a portion of the parts 
supplied by one or more of the branches of the nerve— 
according as to whether it is an irritative or a paralytic 
lesion. The corneal reflex may be absent. Conjunctivitis 
and even suppurative keratitis may occur, and in Case 15 
there was also loss of taste in the anterior two-thirds of the 
tongue on the same side. Anosmia, due to affection of the 
mucous membrane of the nose, may follow lesions of this 
nerve. Affection of the facial nerve is almost as frequent as 
that of the fifth, and is generally unilateral and peripheral in 
character, and often associated with deafness, due to affection 
of the auditory nerve (vide Case 2). 

The symptoms of affection of the vagus nerve relate 
mainly to the circulation and respiration. Specially charac¬ 
teristic is a rapid change of the pulse; it may be quick, 
slow, or irregular (vide Case 10). Various respiratory dis¬ 
turbances towards the end of life are referred to affections of 
this nerve. The spinal accessory may be affected and give 
rise to paralysis of the soft palate and larynx (vide Cases 13 
and 14). Paralysis of the tongue may occur from affection 
of the hypoglossal (vide Case 23). I have, however, been 
astonished to find that with extensive gummatous meningitis 
affecting the whole base of the brain one may have only one 
cranial nerve partially paralysed, and yet on microscopical 
examination one finds extensive infiltration of the nerves by 
a large amount of inflammatory material 

Basilar meningitis frequently gives rise to polydipsia and 
polyuria, which may last days or weeks, or occur only 
periodically. Naturally the urine is of low specific gravity, 
and the quantity per diem may vary, it is said, from three to 
ten litres. 

The condition was only observed in two of my cases 
(vide Case 5), whereas Oppenheim states that it is a 
frequent phenomenon ; but my cases were observed either in 
the out-patient department of the hospital or in the asylum. 
Such a condition might easily have been overlooked. It has 
been ascribed to an affection of the vaso-motor centre of the 



floor of the fourth ventricle by some authorities, by others to 
an affection of the vagus. Diabetes mellitus occasionally 
occurs also; there may he loss of appetite, and nutrition 
sometimes fails. On the other hand, when dementia occurs, 
the appetite is sometimes voracious (vide Case 35). This 
patient would steal his neighbour’s food ; a symptom which 
is looked upon by the attendants as very characteristic of 
general paralysis. Case 5 had a very good appetite and 
became unusually fat when the acute symptoms subsided 
under treatment. There is usually constipation. There 
may be paresis in the limbs, but as a rule, unless there be 
blocking of an artery, there is not paralysis. Case 45 was 
an exception, but this was one in which spinal irritative 
phenomena presented themselves in the form of tetaniform 
spasms with opisthotonos. 

Psychical symptoms .—None of the cases which I have 
examined post mortem have been simple meningitis; they 
have all been associated with very marked changes in the 
arteries, and the mental symptoms which they showed were 
very probably due to circulatory disturbances as well as to 
the meningitic process. Heubner showed that when two 
large branches entering into the formation of the circle of 
Willis are profoundly affected by the obliterative arteritis, 
mental symptoms arise. In the cases which I refer to, all 
the arteries were more or less affected and the circulation in 
the whole brain would be partly affected by hindrance to the 
flow of blood to the hemispheres, owing to the obliterative 
process, and also in some degree to the loss of elasticity of 
the vessels. Moreover, most of the cases show that these 
severe forms of the disease that come into the asylum sooner 
or later develop the formation of gummatous masses, and we 
have to consider, therefore, the effect of these new growths 
in the brain and also the effect on the intra-cranial pressure. 
Still, several gummatous tumours may exist in the cranial 
cavity, as in the cases recorded, without producing as marked 
symptoms of intra-cranial pressure as a small rapidly- 
growing tumour would do. It may be that while the 
gummatous process advances, atrophic changes occur in 
the brain and less blood enters the organ by the arterial 



system, owing to the obliterating process in the arteries, 
and thus increased intra-cranial pressure is not so readily 
brought about; but some of the cases, for example, 35, 
may develop gummata so rapidly that intra-cranial pressure 
and consequent choked disc occur. The effects of arterial 
occlusion will be more fully discussed later on. 

Disturbances of consciousness play a most important role 
in the symptomatology of basic syphilitic disease. One of 
the commonest symptoms is somnolence with a kind of 
drunken stupor, from which the patient is with difficulty 
aroused (vide Cases 25, 30, 44). 

Associated sometimes with this condition is a purposeless 
motile activity and restlessness. Such patients may respond 
to questions or not, and are usually wet and dirty in their 

The stupor may deepen, or the patient may become quite 
conscious again (Cases 5 and 39 onwards), and it might 
be hoped, therefore, that he is about to recover, when 
quite unexpectedly the drowsy stupor will again come on 
and perhaps deepen to coma, and the patient dies without 
regaining consciousness. 

Reference to the article upon three cases of tumour of 
the 3rd ventricle shows that this condition is not peculiar to 
syphilis, but that it is probably due to circulatory disturb¬ 
ances in the brain. Recurrent attacks of drowsiness, 
stupor and coma should always make one suspect basic 
syphilitic meningitis. In the drowsy condition the tonus of 
the muscles remains and the reflexes are present, but as the 
coma deepens both may be lost. In all the cases of severe 
brain syphilis, dementia is a constant symptom, and all 
stages between slight impairment of intelligence and gross 
dementia may be met with. This condition varies with the 
individual at different times, and the variability of the de¬ 
mentia is especially characteristic of the disease. It may 
happen that delirium with acute maniacal excitement may 
be the first indication of mental symptoms, or loss of temper, 
moroseness and excitement may usher in the symptoms. 
Sometimes such a patient is found wandering at large 
(vide Case 39). 



A frequent condition in these cases is mental depression 
with delusions of persecution and attempt at suicide, and 
these patients are dangerous to themselves and others. 
Alternating with mental depression one frequently finds 
mental excitement, and such disturbances may alternate with 
comatose attacks and with periods in which consciousness 
is only partially disturbed, and the intelligence is fairly 
good. Epileptiform fits may arise in such cases, and a 
patient consequently may assume at one time the symptoms 
of an epileptic, at another a general paralytic, or an imbecile, 
or the case may be diagnosed as mania or melancholia ; and 
we can understand that without a proper history of the 
course of the disease prior to admission, how difficult the 
diagnosis becomes. 

The convulsions may be epileptiform in type, generally 
and frequently attended by simple loss of consciousness, 
which may last a few minutes, a few hours, or a few days. 
Clonic spasms, partial or unilateral, with consciousness 
slightly or not at all disturbed, may come on, but as a rule 
the fits are transitory and not persistent; they are due 
mainly to affection of vessels or to softening near the motor 
tract (vide Cases 1, 2, 3, 37, 41, 52). 

When Jacksonian epilepsy occurs in syphilis it indicates 
a gumma or gummatous meningitis of the cortical motor 
area. Tetaniform spasms, with opisthotonos, occasionally 
occur in the severe forms of cerebro-spinal meningitis, and, 
according to Wunderlich, a cataleptic state may occasionally 
be seen. Most of the cases, when admitted to the Asylum, 
showed motor paresis and exaggerated deep reflexes on one 
or both sides; some had obvious hemiplegia, but in one 
(Case 5), an attendant, whom I saw in the earlier stages of 
the disease, the knee-jerks were absent. Sometimes syphi¬ 
litic brain disease may be combined with alcoholic neuritis, 
and on that account the knee-jerks may be absent. 

A great many of the cases which died in the Asylum 
were diagnosed as general paralysis, and certified as such 
after death. It is, however, essential to differentiate this 
pseudo-general paralysis, for it is a totally different disease. 
Should a patient recover—and many do partially recover 


under suitable treatment—they are left mentally enfeebled; 
the expression of the countenance shows a feeble mind; 
there is lack of expression and fixity of gaze, which denote 
absence of the normal stimuli influencing the tone of the 
muscles of expression; the patient’s speech is slow, often 
thick and slurred, Bradyaphasia, dysarthria, but seldom com¬ 
plete motor aphasia {vide Cases 13,24,33,36, &c.). There is 
weakness of memory, slowness of thought and action, loss 
of will power, often a stolid indifference with a tendency to 
causeless outbursts of passion, even of cheerfulness or 
mirth. He is emotional and easily moved to tears and 
laughter, and, generally speaking, there is loss of the 
highest controlling influence of the brain. Sometimes 
there is a permanent ocular or other cranial nerve paralysis, 
blindness or deafness, monoplegia, hemiparesis, hemiplegia, 
dysarthria or general paresis. 

Syphilitic Diseases of the Brain Convexity. 

A hard and fast line cannot be drawn between syphilitic 
disease of the base and of the convexity; several of the cases 
upon which I made the autopsies showed that both the base 
and the convexity were affected. 

There are two forms—(a) Circumscribed; (6) Diffuse. 
The process may start in the bone or in the meninges, and 
spread thence to the brain, causing meningo-encephalitis. 
Several of these cases I have recorded, and they have some¬ 
times followed a blow on the head which sets up an inflam¬ 
mation either in the bone or in the membranes, at a definite 
spot; jtfst as a blow on the shin may cause a periosteal node 
in a syphilitic person, and this node, we know, may undergo 
regressive metamorphosis. The specific inflammation of the 
meninges causes extremely severe pain, paroxysmal in char¬ 
acter ; and, besides general headache, there is usually a well- 
defined localised tenderness on pressure or percussion {vide 
Cases 7 and 8), which may be independent of spontaneous 
headache. The general symptoms of meningitis of the 
convexity may be vomiting, stupor, giddiness and psychical 
disturbances. If, however, the process is circumscribed and 



situated over a “ silent ” part of the brain, headache may 
for a long time be the sole symptom. 

Optic neuritis is uncommon ; it may, it is said, even be 
absent when nearly the whole of the one hemisphere is 
affected; several cases show that the most severe brain 
syphilis may for a long time be unattended by any changes 
ophtbalmo8copically. Gummatous growths on the convexity 
produce definite localising symptoms when they are seated 
in certain parts of the brain, e.g., over the motor area (vide 
Cases 7 and 8), in which the case was diagnosed and cured. 
If, however, the case is not diagnosed and not treated, e.g., 
Cases 86 and 53, scar tissue is formed which cannot be 
absorbed by iodide, and epilepsy is permanently established. 
Some of these cases would doubtless benefit by operation. 

The gumma may be seated over Broca’s convolution and 
give rise to affections of speech and dementia which may be 
erroneously diagnosed as general paralysis (vide Cases 33 
and 36). The motor aphasia usually begins as a transitory 
symptom lasting for a period of time varying from a few 
minutes to an hour or two; the patient may be completely 
aphasic or only have a difficulty with the utterance of 
words; speech may suddenly return ; sometimes the speech 
disturbance is associated with paraesthesia of the right half 
of the body. The loss of speech is frequently preceded by 
a tingling sensation in the facio-lingual area (vide Cases 1 
and 32). 

Certain cases show complete aphasia lasting weeks or 
months, followed by a permanent speech defect; but even 
then the speech disturbance (vide Cases 36, 33, 39) may 
vary considerably at different times, and only exceptionally 
reaches a complete and total aphasia. Complete aphasia is 
always accompanied by facio-lingual paresis or paralysis, 
together with hemiparesis or hemiplegia (Cases 33 and 

The Case 53 was most instructive, for she was shown to 
me as an epileptic with dementia. She had had old left 
hemiplegia affecting the leg and arm with ankle clonus and 
contracture; left pupil dilated and fixed. The post-mortem 
showed an old gumma in the upper part of the motor area 


of the right hemisphere and another in the top of the left 
occipital lobe. 

Case 48 was instructive, for it showed auditory halluci¬ 
nations and epileptiform convulsions. In this case the 
gummatous process had caused an adhesive meningitis of 
the first temporal convolution, thus explaining the auditory 

The two cases (8) of injury to the skull followed years 
after by severe headache, with symptoms of chromatopsy, 
although in only one case a syphilitic history was obtain¬ 
able, were both cured by anti-syphilitic remedies, and were 
therefore probably due to gummatous meningitis affecting 
the occipito-angular region. 

When the gamma occurs over those portions of the brain 
which Flechsig terms “ Association Centres,” it would be 
difficult to diagnose the existence of the same, for, although 
psychical disturbances might be produced, the symptoms 
would be too indefinite to be of much value; but the ex¬ 
istence of severe headache, especially if accompanied by a 
history of syphilis, local tenderness, and with or without 
the history of a blow, should, according to practical experi¬ 
ence, determine the physician to try anti-syphilitic remedies, 
as success in the above two instances has shown. There 
may be sensory disturbances in the disease- of the con¬ 
vexity and paralytic symptoms such as hemiplegia. 

Charcot considers cortical epilepsy to be one of the 
commonest results of brain syphilis, while Naunyn found 
only 3 per cent, in over 300 collected cases. Without a 
post-mortem examination statistics are not very reliable, and 
should the post mortem be made some long time after the 
onset of the disease, regressive changes may have occurred 
to such an extent, especially if iodide has been given, that 
although the fits, at first localised, have been followed by 
general convulsions indistinguishable from epilepsy, little is 
left behind to show the original meningitis which gave rise to 
the initial symptoms. I feel convinced I have seen several 
of these cases. 

Diffuse meningitis and meningo-encephalitis have been 
described. Some of the cases reported were probably cases 



of general paralysis, for the authorities who have described 
this condition have sought to differentiate it from general 
paralysis by the absence of grandiose delusions, but we 
know that a large number of cases of general paralysis do 
not show this symptom, and that there are many atypical 
forms of the disease in which forced movements, tonic 
spasms, epileptiform convulsions of a Jacksonian type, 
active contracture and stiffness of the neck with retraction 
occur. I have seen several such cases, in which at post¬ 
mortem nothing else was found except the ordinary naked- 
eye changes of general paralysis. Anyone who had not seen 
a great number of cases might easily think they had to do 
with a diffuse meningo-encephalitis, especially if there were 
signs of syphilis on the body. I have, however, recorded 
two cases (49 and 52), and I have seen several others like 
these, which neither clinically nor by macroscopical or micro¬ 
scopical examination of the nervous system could be looked 
upon as examples of general paralysis, although there was 
very marked atrophy of the brain and spinal cord, with 
patchy thickening of the membranes. I consider these to be 
true primary meningo-encephalitis with secondary atrophy 
of the neurons as distinguished from general paralysis, 
which I regard as primary atrophy of the neurons with 
secondary meningo-encephalitis. They are due to syphilis, 
and sometimes there is a history of plambism; they are 
chronic, and the dementia is not so progressive nor so 
marked as in true general paralysis. 

Syphilitic Arteritis. 

As we have seen, meningitis whether in the diffuse form, 
affecting the base, or the localised form, or multiple gum- 
mata, is always associated with changes in the arteries, 
either general or local; but arteritis may occur without any 
meningitis. The disease affects especially the inner coat, 
causing narrowing of the lumen of the vessel. Unless this 
affects one large trunk such as the basilar or two adjacent 
branches of the circle of Willis, no obvious symptoms may 
arise unless thrombosis in the vessel takes place. We shall 


first consider those cases in which the vessels are generally 
affected by an obliterative arteritis, but without occlusion by 

A vessel may be almost or even completely blocked by 
proliferation of the inner coat—sufficient, in fact, to cause a 
temporary loss of function of some portion of the brain and to 
give rise thereby to transitory symptoms denoting temporary 
circulatory failure, but not necrosis of a portion of the brain 
with a definite function. As soon as collateral circulation is 
restored by patent collateral vessels, the function returns; 
this should be a warning not to be neglected, for with each 
return of the symptom, the danger of permanent destruction 
increases, until sooner or later collateral circulation is no 
longer possible, and owing to spread of the obliterative pro¬ 
cess the part becomes permanently deprived of blood and 
undergoes necrosis. If it were not for the fact that the 
vessels are generally extensively and progressively affected 
there would be less danger of non re-establishment of 
the collateral circulation. Dr. Leonard Hill has shown 
that both vertebral arteries and both carotids may be 
ligatured in a dog, and he has found that the animal is then 
paretic and demented, with psychical blindness and deaf¬ 
ness ; but in a very short time it regains all its functions and 
behaves exactly like a normal healthy dog. Collateral 
circulation has been re-established by the anterior spinal 
arteries which become as large as vertebrals; he has also 
found that the dog’s brain, before collateral circulation is 
completely re-established, is excitable, even hyperexcitable, 
and that stimulation of the crucial sulcus with a moderate 
current sometimes produces a fit. The transitory character 
of the symptoms in syphilitic arteritis may be explained by 
temporary circulatory disturbance. The most usual seat of 
arteritis is the Sylvian fossa, but the basilar artery is often 
also affected as well as the other branches of the circle of 
Willis. I have frequently found the lenticulo-striate arteries 
affected by nodular arteritis when other vessels have not 
been so diseased (vide Cases 37, 38, 42, 43, 45, 46, 47). 

Symptomatology .—Occlusion of the arteries is almost 
always preceded by premonitory symptoms of which head- 



ache is one of the most important; in fact, this symptom 
may exist for months or years before other symptoms arise 
{vide Case 42, where only the vessels were affected as proved 
post mortem.) This is especially the case when the basilar is 
affected, as in 42, and in a case recorded by Oppenheim, as 
well as Anderson’s case recorded by Hutchinson. The 
headache may be very severe, usually much worse than in 
arterio-sclerosis, but it does not reach the same intensity as 
that of meningitis ; it is, however, sometimes associated with 
meningitis (42). There is generally giddiness and stupor, 
together with physical and psychical disturbances closely 
resembling general paralysis (vide Cases 37, 38, 42, 43, 45, 
46, 47): sleeplessness, irritability, weakness of memory 
and intellect may also be premonitory symptoms. The 
transitory character of the early phenomena of syphilitic 
arteritis before thrombosis has occurred is a very important 
feature. It can be understood that if one or more of the 
large arteries be occluded, considerable variations of the 
blood supply and blood pressure in the hemispheres may 
result; and this would account for fainting fits and loss of 
consciousness like a true apoplectic seizure or the seizures of 
general paralysis. Often one of the earliest symptoms (vide 
Cases 1, 24, and 32) is a transitory aphasia, as Charcot 
pointed out; sometimes it is loss of memory of words, but 
there may be all forms of speech defects; this transitory 
trouble in speech may occur several times in the day. There 
may be in other cases temporary word blindness, or word 
deafness, or other forms of disordered vision or hearing; or 
the first symptoms may be a transitory monoplegia, or hemi¬ 
plegia, or hemiparesis, ushered in by numbness or tingling 
of the part. The paresis or paralysis may last perhaps a 
few minutes, a few hours, or a few days, and then it dis¬ 
appears again to return, and eventually ends in permanent 
loss of function. Sometimes the patient can describe 
exactly the onset of the paralysis or aphasia, but usually at 
that time there was giddiness, or dulness of perception, or 
somnolence, and these symptoms sometimes exist after the 
paralysis has passed off. It is much more common to find 
loss of motor power than loss of sensibility, but various 


sensory phenomena may occur, such as pain, paresthesia, 
hemianesthesia, hemianopsy. Frequently there is paralysis 
of cranial nerves, generally associated with hemiplegia. 
Dysarthria is not unfrequently met with in association with 
difficulty in swallowing and bulbar symptoms {vide Case 13), 
indicative of disease of the basilar or vertebral arteries. 
Alternate hemiplegia is another symptom of basilar disease. 
Various difficulties of speech, namely, a curious drawling, 
staccato speech, without any distinct paralysis of the muscles 
of articulation, have been found associated with multiple 
softening of the hemispheres of a widespread nature. 
Syphilitic arteritis may produce hemiplegia of one side of 
the body and a partial recovery still take place. Then 
one limb or the face on the opposite side may be affected 
and become paralysed, so that, while the disease is clearing 
up in one part, it may be progressing in another, and 
this protean aspect of the disease is very characteristic. 

A number of cases of syphilitic arteritis live a consider¬ 
able time partially or wholly incapacitated by mental affec¬ 
tions associated with paralysis or either condition separately, 
although it is rare not to find some degree of both. On the 
one hand, those in which the paralytic symptoms are 
predominant become patients at the general hospitals for a 
time, and eventually drift into the workhouse infirmaries, 
where either they die after a variable period from the brain 
disease itself or some intercurrent complication, or they 
become sooner or later either so demented as to be cer¬ 
tifiable lunatics, or they develop maniacal or melancholic 
symptoms which necessitate their removal to an asylum 
(vide Case 49). On the other hand, cases in which the mental 
symptoms predominate from the first are usually immediately 
transferred to the asylum, and a diagnosis is then frequently 
made referring to the mental symptoms rather than the 
organic cause of the disease. These patients often live a 
long time (Case 28), and at the autopsy one may find chronic 
disease of the arteries of an obliterative character, some¬ 
times attended with gross naked-eye patches of softening, at 
others only with miliary softenings. The softened area may 
not have destroyed completely the motor pyramidal system 



in a hemisphere; a hemiparesis or a partial hemiplegia may 
exist owing to the existence of patches of softening in the 
hemisphere, either in the anterior part of the capsule or in 
the frontal region of the brain, causing irritation of the 
cortical pyramidal system and giving rise at first to epilepti¬ 
form fits, which afterwards become generalised and indis¬ 
tinguishable from true epilepsy {vide Cases 37, 41, 43, 51). 
Such patients are classified in the asylums as epileptics, but, 
like the epilepsy that so frequently follows congenital or 
infantile cerebral hemiplegia {vide Case 29), it is of organic 
origin and should be entirely differentiated from true 
idiopathic epilepsy. 

In the pathological section of this article the condition 
of the arteries in these old cases of syphilitic brain disease 
and their relation to atheroma and arterio-sclerosis is dis¬ 
cussed, but I may say here that a large experience and a 
very careful attention to the subject has convinced me that 
syphilis plays a very important part in the production of 
atheroma and endarteritis deformans of the nodular 
character as distinguished from arterio-sclerosis, where 
there is a universal thickening of the endarterium secondary 
and compensatory to weakening of the muscular and elastic 
coats. I have found that many of the chronic syphilitic 
cases show a condition of the arteries which would be called 
atheroma by some authorities, hut the morbid process 
always tends to the obliteration of the lumen of the vessel; 
consequently, I attribute many of those cases of early 
universal degenerative changes of the arteries occurring in 
persons between 40 and 50 and associated with symptoms 
like those of general paralysis (and, indeed, often associated 
with the true primary degeneration of the neurons, which I 
hold to be the essential factor in general paralysis), as of 
syphilitic origin. I have not yet seen a case of tabes with 
hemiplegia, but such cases due to syphilitic arteritis do 
occur, according to Minor, and the condition is undoubtedly 
rare. 1 However, I have seen cases of general paralysis pre¬ 
ceded by coarse paralytic symptoms {vide Case 56), found, 

1 Since writing the above I have seen a case of right hemiparesis followed 
by tabes (Case 59). 


post mortem , to be due to syphilitic endarteritis. A con¬ 
siderable number of cases of general paralysis, however 
(found by very careful examination of all the arteries), 
show typical nodular endarteritis, insufficient, however, to 
produce coarse paralysis or symptoms during life. Such 
being the case, the question naturally arises whether a good 
number of those cases of multiple softening and chronic 
brain degeneration associated with degenerated arteries and 
which are numerous in asylums would arise if it were not 
for syphilis. Such patients develop symptoms of premature 
senile mental decay between 45 and 50 years of age (i vide 
Cases 46, 47). 

It is often supposed that because the symptoms do not 
yield to anti-syphilitic remedies therefore they cannot 
be of syphilitic origin. It is well to point out here what 
Gowers so strongly emphasises, that iodide of potassium 
and mercury only do good in removing neoplastic formations, 
such as gummata, meningitis and the early stages of 
arteritis. It cannot be supposed that brain tissue can be 
regenerated when softening has taken place, nor can it be 
supposed that the scar tissue in diseased arteries or the 
atheromatous processes of degenerated arteries can be in¬ 
fluenced by drugs. It is not, however, denied that their 
administration may prevent progress of the disease and thus 
allow other parts of the brain to take on function to some 
extent. Again, it is not to be supposed that the cases must 
necessarily show skin lesions or external bodily signs of 
syphilitic residua, for Fournier has shown that among the 
tertiary manifestations of syphilis, skin lesions or rashes are 
less frequent than diseases of the nervous system. Out of 
3,429 of his cases of syphilis presenting symptoms in the 
tertiary stage there were 787 skin affections and 1,085 
affections of the nervous system. 

Cerebro-Spinal Syphilis. 

Nearly all the cases of basic syphilitic meningitis which I 
have examined post mortem, and microscopically have, as I 
have said before, shown evidence of the spinal membranes 



having been affected to some extent. As a rule, the brain 
symptoms are so predominant that the spinal symptoms are 
overlooked. Some cases, however (e.g., 45,10,18), exhibited 
symptoms during life—stiffness in the neck, pains in the 
back, radiating pains, girdle sensation with hypersesthesia 
over the buttocks, trunk, or extremities indicative of inflam¬ 
mation of the posterior roots; likewise, atrophic paralysis, 
as in Case 18, indicates affection of the anterior roots. In 
some cases there is ataxy and disturbances of the sphincters, 
together with paresis of the extremities, sometimes all four, 
sometimes one or more, the greater number of cases being 
limited to the lower extremities. 

Erb has described a form of syphilitic meningo-myelitis 
which according to Oppenheim is only a form of cerebro¬ 
spinal meningitis; it causes paraplegia and the onset is 
usually gradual and not related to exposure to wet and cold; 
in fact, it comes on spontaneously. It is, however, remark¬ 
able in the fact that it usually begins within the first few 
years after infection. Of six cases which have come under 
my observation, one occurred in the first year, two in the 
second year, two in the third year and one in the eighth 
year after infection. One case was fatal from septic infection 
of a large bedsore with secondary pneumonia complicated 
by cystitis and suppurative nephritis, four recovered com¬ 
pletely under treatment and one remained permanently 

One case, E. M., was remarkable, inasmuch as he had 
been under treatment three years at the Lock Hospital ever 
since the initial infection. One case, K., seven years after 
infection developed symptoms of basal meningitis, namely, 
strabismus, double vision, ptosis, severe headache, loss of 
memory, drowsiness, nausea and vertigo. He recovered 
completely under treatment, but returned a year later with 
girdle sensation in the seventh left intercostal space and 
slight numbness in the foot. A week later he became com¬ 
pletely paraplegic, with loss of sensibility, exaggerated deep 
reflexes and loss of voluntary control over the sphincters. 
In ten weeks he recovered completely under treatment, and 
the interest about this case is that he first had symptoms 


a year before of basic meningitis. Tbe case that died was 
seen in Charing Cross Hospital ten years ago. I fully 
expected to find a gumma at the post mortem, but careful 
microscopical examination of the cord showed a focal 
myelitis in tbe mid-dorsal region with descending and 
ascending degenerations, but not following regularly any 
definite systems. The membranes in the mid-dorsal region 
were infiltrated with leucocytes, especially around the veins. 
That the dorsal region is the usual seat of the focal myelitis 
may be accounted for by the fact that in this situation the 
circulation is most precarious; it is therefore the position 
in the spinal cord where stasis is most likely to occur. 
Some authorities wish to associate this condition with 
excessive use of mercury. In three of the cases on the one 
hand, which I have notes of, the patients had been on 
mercury for a considerable time; on the other hand, three 
had had no mercurial treatment, and two of them rapidly 
recovered when given it; moreover, in the case K. referred 
to, the mercurial treatment with iodide was continued and 
he made a most satisfactory recovery. In fact, my some¬ 
what limited experience is opposed to the view that mercury 
causes this affection; rather would I believe the converse 
that lack of treatment leads to this specific affection of the 
spinal cord As it does to cerebro-spinal meningitis, although 
in some cases after most efficient treatment the disease may 
manifest itself just as we have seen it sometimes does in 
cerebral syphilis. 

Note. —These spinal cases are not included among the 
cases recorded in Appendix. 


The cases of brain syphilis which have been investigated 
post mortem in this series show that the lesions are varied 
and manifold; essentially the process is an inflammatory 
one affecting the mesoblastic tissues starting either in the 
membranes or in the walls of the blood-vessels, frequently 
affecting both and giving rise in many instances to new 
formations—gummata of Virchow, syphilomata of Wagner. 



The symptoms depend upon the seat of the inflammatory 
process, which may be local or general. The gummatous 
process may be either circumscribed or diffused : frequently 
the two are combined; the diffuse form of gummatous 
meningitis was met with frequently, and generally associated 
with arteritis ; usually the inflammatory exudation extended 
into the Sylvian fossa on each side along the vessels, and 
from there into the substance of the brain; it also extended 
down the spinal cord. 

Twenty-three fatal cases are recorded in which a careful 
microscopical examination was made. This includes all the 
severe cases of brain syphilis which have occurred at Clay- 
bury Asylum during the last few years and two from 
Hanwell. By severe brain syphilis I mean multiple gum- 
mata or cerebro-spinal meningitis. I have only described a 
few selected typical cases of the other pathological conditions 
caused by syphilis. An analysis of the macroscopical and 
microscopical character of the lesions allows the following 
classification to be made :— 

1. —Multiple syphilitic lesions. 

(а) Cerebro-spinal meningitis (usually termed basic 
meningitis), multiple gummata, and arteritis. 

(б) Cerebro-spinal meningitis associated with arteritis. 

2. —Localised circumscribed gummata. 

3. —Universal occluding endarteritis. 

(a) Causing mental symptoms by failure of nutrition. 

(b) Associated with the characteristic primary decay 

of neurons, typical of general paralysis. 

(c) Nodular arteritis, partial, causing softening either 

by occlusion or thrombosis. 

(d) Ectasial arteritis causing aneurism. 

4. —Relation of syphilis to atheroma and arterio¬ 

Multiple syphilitic lesions .—This severe and frequently 
intractable form of the disease is especially liable to occur 
soon after infection. Most of the cases in which a history 
was obtained showed that it came on within the first two or 
three years after infection. Many of these cases acquired 
the disease while in the services abroad. It may, therefore. 


be considered possible that the effect of the virus varies 
according to the source; but probably individual idiosyn¬ 
crasy plays even a more important part {vide cases of two 
brothers, 16 and 17). Morel Lavalle has related an instance 
where a number of people infected from the same source 
suffered from severe nervous affections. 

It is well known, and the cases recorded confirm the 
opinion, that the virus is especially liable to affect the inter¬ 
peduncular space at the base of the brain. The cases I 
have examined also show that the disease spreads up the 
Sylvian fissures and down the spinal cord, and not usually 
on to the convexities of the hemispheres. This is exactly 
where the cerebro-spinal fluid exists in abundance in the 
cranio-spinal cavity. This fluid no doubt functions as the 
lymph of the brain, and is contained also in the ventricles; 
these cavities communicate with the subarachnoid space 
by the foramina of Magendie. Inflammatory exudation 
about the base of the brain would tend to close this com¬ 
munication and interfere with the escape of the fluid 
from the ventricles, thereby causing internal hydrocephalus. 
This condition may account for the stupor, drowsiness, 
paresis and dementia, with intervals of comparative mental 
sanity; which alternate states may be coincident in the one 
case with accumulation, in the other case with absorption 
or escape of the retained fluid. Very probably when the 
fluid pressure in the ventricles equals that of the venous 
pressure, secretion of the choroid plexus ceases. 

If it be admitted that the virus finds a suitable soil for 
its development in the cerebro-spinal fluid of the cranio¬ 
spinal cavity (just as we know tubercle does) we can easily 
understand why I have found in all these cases that the 
process, although most intense in the interpeduncular space, 
has spread to the Sylvian fissure and throughout the whole 
spinal canal and not to the convexities of the hemispheres. 
It may be asked why does it not affect the ventricles ? in 
only one of the cases were there any signs of ventricular 
lesion, and that was found to be due to direct extension of 
the inflammatory process along the perivascular lymphatics 
of the lenticulo-striate arteries ; but it may be explained by 



the fact that, the ependyma of the ventricles being of 
epiblastic origin, the syphilitic virus causes no formative 
proliferation and has an irritative proliferative influence only 
upon moesoblastic structures. 

Again, we have to consider the possibility of a toxic 
influence upon the neurons by the altered cerebro-spinal 

Naked-eye appearance of brain syphilis. — Essentially 
the change is the same in all cases of brain syphilis ; it is a 
process of inflammation which is termed specific, although 
really there is nothing absolutely specific about it, except 
certain characteristic features which experience has taught 
us to associate with syphilis. If there were a definite 
organism as in tubercle we might call it specific. There is 
considerable resemblance between tubercular and syphilitic 
brain disease—it is often extremely difficult to decide which 
it is. 

This was so in Case 51; only after repeated examination was 
I convinced that the case was tubercular by finding a few bacilli 
in the giant-cells. The naked-eye characters of the new growths 
in this case corresponded much more closely with the classical 
description of gummata by Virchow than with tubercle. Of 
course there is with the syphilitic history the possibility, nay, 
probability, that the case was one of combined tubercle and 

Syphilitic new growths belong to the granulation tumours 
of Virchow or the infective granulomata of Klebs; they are 
termed gummata. The gummatous process, which nearly 
always starts in the membranes, may extend over the surface 
of the brain in the form of an exudative meningitis , or it 
may spread along the vessels into the substance of the brain, 
causing a definite localised tumour . If the process starts 
anywhere about the base, such as the interpeduncular space 
and optic chiasma, it usually spreads into the Sylvian fissure 
and into the whole base of the brain surrounding the vessels 
and branches of the circle of Willis and the cranial nerves, 
forming a gummy exudation which has a semi-solid con¬ 
sistency not unlike agar or gelatine culture media in appear¬ 
ance. The membranous deposit may be removed with the 


finger when of comparative recent origin; when of some 
standing it is dryer and firmer. In colour it may be grey or 
grey and red; it may be semi-translucent or opaque, some¬ 
times yellowish or speckled. Under treatment no doubt 
this inflammatory exudation can in great measure disappear. 
The vessels appear thickened and of a dirty white or yellow 
colour, like wet wash-leather. They can be easily cut 
transversely and the lumen can be seen partially or com¬ 
pletely occluded; the endarterium is markedly thickened, 
usually more on one side than on the other, giving the 
section a half-moon appearance. The vessels may be stiff, 
like cartilage to the feel, but in the acute cases there was 
not this cartilaginous resistance, although the vessels were 
very much thickened. Besides the nodular and general 
endarteritis there is always nodular and general peri¬ 
arteritis. Little nodules visible to the naked eye could be 
seen scattered about the base of the brain; in some of the 
cases these miliary gummata were found microscopically to 
consist of small vessels affected with endarteritis and 
nodular periarteritis, thus resembling miliary tubercles. 

Localised new growths — gummata. —In all the cases in 
which gummata occurred as part of multiple syphilitic 
disease the new growths were not single but scattered about 
in various portions of the brain. In nearly all cases the 
growths appeared to have either started from the membranes 
or the process had proceeded by direct extension along vessels 
into the substance of the brain. When starting from the 
meninges of the hemispheres and of a circumscribed 
character they caused adhesive inflammation to the dura 
mater. Gummata were found in both hemispheres, the 
pons and crura cerebri, the basal ganglia and the lateral 
ventricles, hut not in the cerebellum. In this latter situa¬ 
tion tubercular growths are, however, common (vide 
Case 51). The size varied from that of a pea to a pullet’s 
egg, the most frequent size being from that of a barcelona 
nut to a walnut. They varied much in consistency and 
colour as well as in general appearance. Their consistency 
is usually unequal in different parts, the younger peripheral 
growing tissue being soft, succulent and vascular, the older 



dry, firm and non-vascular; hence the growing edges appear 
grey, greyish-red, or red, while the central portions appear 
yellowish owing to the occurrence of necrotic changes akin 
to caseation. The caseous mass, however, does not usually 
form a defined nodule, but is more often broken up into 
irregular areas which coalesce here and there by strands of 
grey, fibrous, or soft greyish-red granulation tissue. There 
is little tendency to calcification or to break down and form 
an abscess. 

The circumscribed gumma which frequently arises from 
a blow on the head or an injury of the cranium, as many of 
the cases show, starts usually in the dura mater or pia 
arachnoid and causes a circumscribed adhesive inflammation 
of the bone to the membranes and of the membranes to the 
brain. The inflammatory process causes great thickening 
of the dura, but there is little tendency to spread; it is 
usually a tertiary lesion and gives rise to symptoms indi¬ 
cating local rather than general affection of the brain. 
Usually this form of disease, if treated early before generalised 
symptoms have become permanently installed, e.g., epileptic 
convulsions, is the most amenable of all forms of brain 
syphilis to treatment. 

Microscopical Examina tion. 

The neoplastic formation, whether circumscribed or 
diffuse, is essentially the same. It consists of an inflam¬ 
matory exudation product containing enormous numbers 
of round cells indistinguishable from migrated leucocytes in 
a coagulated serous fluid, and this forms the main con¬ 
stituent of the membranous deposit found at the base of the 
brain. It invades all the adjacent structures, the membranes, 
the walls of the vessels, the pial septa and the roots of the 
cranial and spinal nerves; the acute inflammatory process 
causes congestive stasis in the vessels; thus, wherever this 
inflammatory process has extended (independent and apart 
from the organic changes in the walls of the vessels) one 
finds venous and capillary stasis, e.g., in the spinal roots of 
many of these cases there was little or no arteritis, and yet 


all the roots showed extremely dilated and congested vessels 
as if the cerebro-spinal fluid which bathed them had by its 
altered composition caused the inflammation. Besides this 
there is active proliferation of the mesoblastic connective 
tissue elements, and one finds, therefore, numerous spindle 
and stellate cells. In the older parts of the gummatous 
process these formed elements may alone remain, the in¬ 
flammatory products having been absorbed. Such was the 
case in parts of the gummatous deposit of McK. and E. M., 
due no doubt to the iodide treatment they received, which 
had led to the complete absorption of a large gumma on 
the sternum. The changes in the vessels are essentially of 
the same nature, viz., due to infiltration of the walls of the 
vessels with inflammatory products from without inwards, 
periarteritis associated with proliferation of the connective 
tissue elements of the adventitia. This may be general, 
just as the gummatous process affecting the membranes, 
and the vessels then are involved in the gummatous 
meningitis, or it may be more intense at one particular 
spot forming a small periarterial gumma —-periarteritis 
nodosa. The external coat is infiltrated with leucocytes or 
round cells, the lymph spaces distended with serous exuda¬ 
tion, and there may or may not be proliferation of the 
branched connective tissue cells, though this is not so 
apparent as the round-cell infiltration. The middle coat is 
infiltrated with leucocytes and the muscle-fibres are swollen 
up with the serous exudation, and not infrequently they 
present the appearance of having undergone coagulation 
necrosis. Sometimes the vessel is filled with an organising 
or partially organising thrombus, and the lumen is thus 
completely obliterated. Not infrequently in the older parts 
of a gumma the recognition of the existence of a vessel is 
only possible by the crinkled line of the still undestroyed 
elastic lamina lying in an amorphous mass (vide photo¬ 
micro., p. 38). In the more recent younger parts of a gumma 
or gummatous meningitis the lumen of the vessel may be 
partially or completely occluded by endarteritis. 

The thickening of the endarterium is very characteristic 
in the vessels of a gumma, and helps to distinguish it from 


Section.of gammataus tna*s ia Sylvinti fissure, Ca*c 33. Showing almost 
completely obliterated vessel*, ftud recogutobie ve&b&ls only by %h fc/elastic, 
oo&fc Magnification •, ‘ ‘ V . v .j ; , . ^ , 


v ; Art.erip« of oiemuges of the lift from Case 33, showing ofiUteraj%v 
ea&nrteyiC*. Magnificat ion f& 


tubercle. There may not be endarteritis elsewhere, as 
several of my cases showed. Still endarteritis is seen in 
tubercle, and it is not absolutely characteristic of syphilis. 
Giant-cells are sometimes met with in syphilitic gummata, 
but their presence rather points towards tubercle or mixed 
infections, and, although bacilli cannot always be found in 
tubercular caseous masses in the brain, giant-cells would 
lead one to make careful search, and, generally speaking, 
bacilli will be found in them. The red or greyish-red soft 
tissue at the edge of the gumma when this is growing from 
the membranes of the brain consists of round cells, spindle- 
shaped or stellate cells, and is usually at first very vascular. 
This really represents the first change in the morbid process, 
the intensity of the inflammation, the rapid cell proliferation 
and the changes which lead up to occlusion of the nutrient 
vessels set up a process of necrobiosis in the central and 
older parts of the growth, while extension takes place by 
new formation at the periphery. There may be at first 
several independent foci in the same neighbourhood forming 
small neoplastic growths ; then these by the growing borders 
coalesce, so as to form one large growth. Thus, we may find 
on cutting into a gummatous tumour a single irregular 
caseous nodule with soft young tissue around, or a number 
of irregular caseous nodules of varying size coalescing here 
and there, or separated at other parts by strands of fibrous 
or round celled inflammatory tissue. The necrosed portions 
microscopically show little tendency to true caseation, there 
are no fatty crystals and no calcareous particles. It is a 
finely granular amorphous mass staining very badly with 
logwood, and shows no trace of structure except sometimes 
the outline of the coats of vessels. 

The changes seen in the vessels depend on the age of the 
process. All the vessels are affected, small as well as large, 
by the acute inflammatory process. All the coats are 
infiltrated with leucocytes, and the thickening of the walls 
may be increased to such a degree as to cause partial or 
complete obliteration of all the small arteries or arterioles 
of the affected membranes. The walls of the veins are like¬ 
wise affected but the process does not produce such an 


/ . . _ . • 

obliteration of the lumen. The blood seen in the trap see - 

lions of the vessels contains an enomious increase of leuco¬ 
cytes corresponding in every respect with the leucocytes in 
the coats of the vessels and adjacent tissues {vide photon 
micro. 3 ). The. vessels that extend into the substance of the 
brain are surrounded by perivascular lymphatics, and we 
can observe the direct of fhe disdasle along these 

i%oTOAuenoaiupH 3* 

Sfef\&i.oi5 of & wm) in e itow Csse B9. '^Ws 

uafrUration of t)m midclJa and Eternal trial'*, \yiirh a #rmt 

immms of ituoocytes hs itjs fcooWimid ;m $(#>« 

lymphatic spaces by-the existence of crowds of leucocytes 
eUrrbuhdmg vessels in which the blood has become stagnant 
or the circulation greatly slowed, and this- condition cannot 
be without infiaeoce upon fcbe structure and functions of the 
.adjacent- braid tissue, causing irritation at.Ttrst and ftHally 
loss of fufltddoih•#their processor deriving 
their nutrition from the vessels so affected, .undergo at Srst 
functional changes, microscopical evidence of which is 


afforded by the alteration in the appearance of the chromatic 
substance, the situation and size of the nucleus—the shape 
of the cell body, and the appearance of the dendritic pro¬ 
cesses. It is a process of inflammatory oedema of the cell. 
The body swells up—the pericellular space is dilated, the 
granules of -Nissl are replaced by a fine dust, the nucleus 
may he swollen and eccentric, the dendritic processes are 
imperfectly seen, and the chromatic spindles on them are no 
longer observable;—changes identical with what L. Hill 
and I have observed in experimental anaemia of animals in 
which there is venous engorgement and arterio-capillary 
anaemia. Should, however, collateral circulation be estab¬ 
lished and the temporary venous stasis removed, the cells 
return to their normal condition after a time, and function 
is restored. The establishment and retention of collateral 
circulation, however, depends upon the extent and the 
intensity of the inflammatory process and the adoption of 
early and vigorous antisyphilitic treatment, which, although 
not able to restore new nerve cells when once they are 
destroyed, is nevertheless able to prevent the extension of 
the vascular disease. The limits of the collateral circulation 
in monkeys is much narrower than that in dogs, and there 
are in animals individual peculiarities as in man. Whereas 
in dogs collateral circulation is invariably established after 
ligation of all four cerebral arteries—monkeys, probably on 
account of the influence of gravity and their semi-erect posi¬ 
tion, cannot live after four arteries are tied: and some of the 
animals had softening of the brain and destruction of the 
nerve cells after ligation of two carotids and a vertebral, 
dying with epileptiform convulsions. 

Venous stasis, together with distension of the perivas¬ 
cular lymphatics and ventricles by cerebro-spinal fluid altered 
in many ways, plays an important part in the symptom¬ 
atology of multiple syphilitic brain disease, general paralysis, 
and cerebral tumours. This fluid, which represents the 
lymph of the brain, under such conditions contains pro¬ 
bably excess of C0 2 and nucleo-albumens, together with 
products of degeneration, e.g., Cholin. Vide article on 
general paralysis, p. 185. 



The nervous elements are thus deprived of their proper 
nutrient environment, and are surrounded instead by a 
pathological fluid which is contained in the pericellular 
spaces. The nerve cell, like other cells of the body, 
nourishes itself and is not nourished, it behaves like a 
living organism; it is therefore possibly temporarily poisoned 
by this fluid, but not killed—its function is only in abey¬ 
ance. If the process is quite local, the disturbances of the 
circulation and the alterations of the lymph will not be 
sufficient to give rise to general symptoms of affection of 
the brain as a whole, e.g,, stupor, dementia, loss of 
memory and intellect, paresis, general convulsions, &c. We 
know that in syphilitic brain disease such symptoms men¬ 
tioned above may exist temporarily, and they may dis¬ 
appear and reappear. Why is this ? In general paralysis 
the dementia is always slowly and steadily progressive; 
many of the symptoms above-mentioned may disappear, 
e.g., stupor and convulsions, but the patient is always 
demented. I think the answer is plain—in syphilitic brain 
disease we may be dealing with loss of function dependent 
entirely upon changes outside the nerve cell itself; remove 
these conditions in time, before death of the nervous tissue 
has occurred, and the nerve cells recover their functions. 
In general paralysis there exists an entirely different morbid 
process, a primary progressive decay of the nerve cell which 
ontogenetically and phylogenetically may be looked upon as 
a regressive metamorphosis, a degenerative process which 
starts in the highest and latest phylogenetically developed 
structures, e.g., the centres of verbal and written speech ; the 
molecular layer with the tangential system of fibres and the 
association systems of the frontal and parietal lobes. This 
premature decay of the highest controlling structures is pro¬ 
gressive and cumulative, it causes phenomena of irritation, 
manifested by mental and physical symptoms, such as motor 
irritation, with rise of blood pressure, cerebral anaemia and 
venous stasis, local and general auto-intoxication respectively 
by the products of degeneration and imperfect metabolism. 
A vicious circle is established which continually is enlarging. 
Some of the general symptoms in this disease, e.g., stupor 


and congestive seizures, may be relieved by free purgation, 
emptying the bowels thus relieving the general venous 
congestion; but the disease itself cannot be attacked. 
Nothing that we know of can rejuvenate the dying and dead 
nerve cells, and seeing that they are perpetual elements 
they cannot be regenerated. But with syphilitic brain 
disease it is different, although the symptoms may so closely 
resemble general paralysis that even some of the best and 
mo6t experienced authorities speak of a syphilitic general 
paralysis. Clinically syphilitic brain disease may frequently 
resemble general paralysis, but not pathologically. The 
former is a disease affecting primarily mesoblastic tissues, 
viz.: the vessels, lymphatics and membranes, with secondary 
degenerative changes in the neuron—the latter is a primary 
decay of the neuron itself with secondary inflammatory 
changes affecting the vessels, lymphatics and membranes, 
due to the irritation of the products of degeneration. 
Nodular syphilitic arteritis is not at all uncommon in the 
vessels of general paralytics if they are carefully searched, 
but it is very seldom that it is sufficient to produce symp¬ 
toms. I have not met with it in any of the cases of juvenile 
general paralysis. It was, however, met with in some adult 
cases, e.g., 55 and 56, and was of sufficient extension and 
intensity to produce symptoms. 

Endarteritis syphilitica .—A digression has been, how¬ 
ever, made from our subject, and we now return to the 
changes in the arteries. Obliterating endarteritis is one of 
the most frequent results of syphilis ; it may be associated 
with meningitis, or not. It affects especially the vessels of 
the circle of Willis, the arteries of the Sylvian fossa and the 
lenticulo-striate vessels. In many of the cases there was 
associated endarteritis and periarteritis, and it was im¬ 
possible to say which was primary, but I incline to the 
opinion that where there is meningitis the periarteritis 
occurs first. The endarteritis is the result of irritation and 
the thickening of the endarterium is brought about by 
proliferation of the sub-endothelial fixed connective tissue 
cell elements ; but the inflammatory exudation and round 
celled infiltration may distend the spaces between the 



stellate and spindle-shaped proliferated cells, and may split 
sometimes the elastic lamina into several films which are 
then separated from one another by the new cellular forma* 
tion, and thus lead to the erroneous conclusion of Heubner 
that a new elastic coat is formed. In some of these cases, 
35, 44, 45, the inflammation was so intense as to give rise 
to the formation of new vessels in the proliferated endar- 
terium, just as the cornea or non-vascular tissue may when 
inflamed become vascularized. If we study the micro¬ 
scopical appearances of the arteries first attacked, and com¬ 
pare them with the more recently affected, we can see a 
marked difference. The former still show a partial or com¬ 
plete obliteration of the lumen, but the acute inflammatory 
process has altered the histological appearances of the 
media as well as the intima; we can no longer clearly 
differentiate the muscle fibres of the middle coat with their 
deeply staining nuclei, the fibres present a homogeneous 
staining, duller in appearance than the healthy media appears; 
very often the whole wall has much the same appearance 
throughout; it looks like dense fibrous tissue with lacunar 
spaces between the fibres. This is what happens when 
syphilis attacks primarily the arteries, except that the 
middle coat, which is nourished by the vasa vasorum, is not 
affected to the same extent as the inner. Heubner main¬ 
tains that syphilitic arteritis never undergoes caseation, that 
it never becomes atheroma. This is certainly not true of 
the aorta; for I have seen a good many cases of nodular 
aortitis occurring in young persons the subjects of syphilis 
under thirty; and I have found in the gelatinous plaques of 
acute syphilitic aortitis, caseation with fatty crystals oc¬ 
curring in the centre of the plaque, due to obliterative 
endarteritis of the arteriae arteriarum. This dictum of 
Heubner is, generally speaking, true, but it is much too 
exclusive; the observations of Oedmannson, confirmed by 
Birsch Hirschfeld, upon the atheromatous changes in the 
umbilical vessels and in the arteries of premature foetuses, 
still-born owing to syphilitic infection from the parents, 
support the contention that atheroma has a direct relation 
to syphilis- I regard marked atheroma of the aorta in young 


persons as strong presumptive evidence of syphilis, espe¬ 
cially when of the nodular circumscribed form. 

In some cases of undoubted syphilis I would venture to 
say that any one looking at sections of some of the smaller 
vessels would without hesitation say that these show typical 
syphilitic nodular endarteritis, while sections of another and 
larger vessel he would call typical nodular atheroma. Cases 
46 and 47 are instances of a large class of individuals who 
about 45 to 50 commence to suffer with various mental 
symptoms due to arterial changes, and I believe syphilis 
plays as important a part in the production of the premature 
degeneration of the cerebral vessels as it does with the aorta. 
It produces this comparatively early degeneration of the 
cerebral vessels in the same way as it does degeneration of 
the nerve-cells in general paralysis, viz., by a devitalising 
influence. I have noticed, moreover, that general paralytics 
who die after 45 very frequently show some degree of 
nodular atheroma of the arteries. The changes in the 
arterial coat convert a living flexible and distensible tube 
into a rigid inelastic pipe, and if many of the arteries of the 
brain are so affected the mechanism of the circulation is 
interfered with. Syphilis is one of the causes of cerebral 
aneurism, but this is comparatively rare. I have only met 
with three cases of cerebral aneurism in the course of three 
years. Two were in syphilitic subjects, but, considering 
the frequency of syphilitic arteritis, aneurism is uncommon. 
In one of these cases it was probably due to embolism 
caused by detachment of fragments from an atheromatous 
ulcer of the -aorta. The other, Case 41, had practically 


The cases that come to the hospital, as a rule, offer lar 
less difficulty than those admitted to asylums. The former 
class of patients are able and usually willing to tell you that 
they have suffered with syphilis, but, even if they will not 
do so, the character and mode of onset of the paralytic 
symptoms, the headache and their age, even without any 
syphilitic residua on the body, and after persistent denial of 



infection, would lead you to suspect brain syphilis, and 
frequently the correctness of the diagnosis is proved by 
rapid improvement under appropriate treatment {vide Cases 
8, 16, 17). 

In women far greater difficulties arise, for they are 
frequently infected by their husbands ; the primary sore is 
often overlooked and also the secondary symptoms ; there 
are often no residua on the body, but parchment scars, 
enlarged cervical glands, evidence of old iritis, and especially 
a collar of pigmentation around the neck should he looked 
for, even when more obvious syphilitic residua or manifesta¬ 
tions are absent. A very important matter is the history of 
miscarriages, abortions, dead foetuses and premature births. 
According to Birsch Hirschfeld, syphilis is responsible for 
two-thirds of such cases. Syphilitic parents may, however, 
have perfectly healthy children. A case of tabes under 
my care was infected as a young man, married subsequently 
and had sixteen children. It depends very much upon the 
severity of the attack and the interval which elapses between 
marriage and infection. Many of the cases recorded showed 
absolutely no traces of the previous infection either in the 
seat of the initial sore or on any part of the body. The 
early cases occurring soon after infection frequently showed 
marked evidence in the form of enlarged glands, rashes, 
scars, &c. The diseases which might be mistaken for 
syphilitic brain disease are:—(1) New growths; (2) tuber¬ 
cular deposit; (3) tubercular meningitis; (4) disseminated 
sclerosis; (5) arterio-sclerosis; (6) epilepsy ; (7) hysteria; 
(8) neurasthenia; (9) alcoholism; (10) uraemia; (11) lead 
poisoning; (12) tabes dorsalis; (13) general paralysis of the 
insane ; (14) mania ; (15) melancholia : (16) epilepsy with 
dementia; (17) softening, local or diffuse, the result of 
embolism or thrombosis, causing paralysis and mental 

Seeing that syphilis may attack any part of the cerebro¬ 
spinal nervous system, causing general or local irritation or 
destructive effects, the syndroma naturally may resemble 
almost any disease of the nervous system. 

New growths , including tubercle. — Some of the cases 


which came under my observation were regarded as being 
probably new growths other than syphilis; the effect of 
treatment showed that, even in the absence of a history of 
syphilis, mercury and iodide should always he tried. New 
growths seldom show the same spontaneous remissions and 
exacerbations as gummatous syphilitic meningitis. This, 
however, proved misleading in the case of H. (tumour of the 
third ventricle, p. 417). He appeared to improve under 
mercury and iodide and showed marked remissions and 
exacerbations, but died with a tumour in the third ventricle. 
Intracranial pressure symptoms, e.g., optic neuritis and 
vomiting, are as a rule, in my opinion, much more severe in 
new growths. 

Tubercular meningitis , although common in young 
children, is relatively rare in adults. I have not met with 
a case on the post-mortem table at the asylums, although 
pulmonary tuberculosis is fairly common. Tubercular 
meningitis is acute and progressive. There are usually 
signs in the lungs of tubercular disease. There is, as a 
rule, more stiffness and retraction in the neck and muscular 
rigidity. The patient falls into a stupor, which deepens to 
coma, and the symptoms are continuous, progressive and 
without remissions. The irritative phenomena precede the 
paralytic phenomena and the pyrexia is more definite and 
continuous than in syphilitic meningitis. Syphilis and 
tubercle may be combined and then syphilitic remedies 
prove useless (vide Case 51). 

Multiple sclerosis .—A differential diagnosis is sometimes 
extremely difficult. Case 43 might have been considered as 
a case of multiple sclerosis. She had nystagmus, speech 
defect, paralysis with exaggerated deep reflexes. Post 
mortem there was a patch of sclerosis in the pons of syphi¬ 
litic origin situated partly in the pyramidal system, partly 
in the middle peduncle of the left side, and combined scler¬ 
osis of the cord. 

Disseminated sclerosis may commence with a symptom 
which is strongly suggestive of syphilis, viz.:—Ocular para¬ 
lysis of one side. Iodide is given and it clears up (probably 
not the effect of the drug, but spontaneous). Such a case 



occurred in my practice, and not long after the patient 
developed all the characteristic phenomena of disseminated 
sclerosis, from which she died. The ocular paralysis in this 
case, however (as it usually is), was of the abducens and not 
the motor oculi, and this is useful to remember. Whereas 
nystagmus is rare in syphilis, it occurs in 60 per cent, of 
the cases of disseminated sclerosis. Pupil symptoms are 
common in syphilis, likewise aphasia, alexia and cortical 
epilepsy. The scanning speech affection of disseminated 
sclerosis should be differentiated from the dysarthria and 
Bradyaphasia of syphilis. Visual affections are common in 
both diseases, but complete optic atrophy and hemianopsy 
are not met with in disseminated sclerosis. It should be 
borne in mind that whereas syphilis attacks the membranes 
first and the cortical and spinal substance later, insular 
sclerosis commences in the white matter of the cerebro¬ 
spinal axis, and therefore meningeal and nerve-root symptoms 
point to syphilis. 

Arterio - sclerosis. —It has already been stated that 
obliterative arterio-sclerosis occurring in middle-aged people 
is, in many cases, of syphilitic origin. This form, I con¬ 
sider, should be differentiated from another form, viz.:— 
general compensatory thickening of the inner coat, secon¬ 
dary and proportional to the loss of elasticity of the mus¬ 
cular and elastic*coat. Certainly, it means the conversion of 
elastic tubes into rigid tubes, and such a pathological 
condition is not limited to the cerebral arteries, but affects 
all the arteries of the body. In this form of the disease, 
various psychical disturbances may arise owing to disturb¬ 
ances in the cerebral circulation, such as fainting fits, 
vertigo, giddiness, mental depression and headache. As a 
rule, however, the headache is much less severe than in the 
obliterative nodular endarteritis of syphilitic origin. A good 
example of this is Case H. N., p. 12]. 

The occurrence of partial, unilateral or universal epilepti¬ 
form convulsions may, as the cases show, be erroneously 
attributed to epilepsy or general paralysis. In fact, it 
seems to be a custom in asylums to regard all fits as 
epileptic or general paralytic. In the majority of cases the 


diagnosis of one or the other would be correct, bat there 
are a certain number due to focal disease, and the recog¬ 
nition of Jacksonian epilepsy in our asylums would he of 
great advantage in the treatment of cases; some of them 
could be cured by iodide of potassium, and a few might be 
operated upon successfully. This, however, can never come 
to pass until the character of the fit is accurately described 
by the medical officer from his own personal observation in 
the case-book. The number of fits is kept account of by 
the attendant, but I have seldom found an attendant able 
to describe to me the march of a fit. I have had cases of 
typical Jacksonian epilepsy due to syphilitic brain disease 
shown to me as cases of epilepsy. 

Case 7 shows how important this is, for here was a man 
who had 400 fits, completely cured by early vigorous treat¬ 
ment. In some cases of general paralysis the fits may have 
a Jacksonian type (vide p. 188), but in all doubtful cases 
vigorous anti-syphilitic treatment should be applied. 

Uraemic fits and the fits due to lead poisoning may be 
mistaken for syphilis, but the history and characters of the 
disease should enable a diagnosis to be made. Not un- 
frequently, however, syphilis is combined with either 
chronic Bright’s disease or plumbism, e.g., Case 49. 

A very difficult problem often presents itself. A man 
who has had syphilis takes to drinking heavily and is sent 
to the asylum. He presents many of the signs of general 
paralysis. He is demented. He has loss of memory, 
especially for recent events, is unable to give any rational 
account of himself, his speech may be affected, his tongue 
tremulous, and there is tremor of the hands. The knee- 
jerks may be absent or exaggerated. He may have mental 
exaltation or depression. All these symptoms may pass 
away when he is prevented from obtaining further alcohol. 
Although the evidence of tertiary syphilis in the form of 
old scars, etc., would make you a little more doubtful 
about your diagnosis, I think, as a rule, it may be said 
that general paralysis is more likely to occur in a patient 
who has had syphilis and who yet presents no tertiary 




The patient, may, however, have unequal pupils, fixed 
to light, and sometimes to accommodation as well. The 
difficulty will thereby be greatly increased, for this is the 
most important early physical sign of general paralysis, but 
it is not pathognomonic by itself. A provisional diagnosis 
should in such a case be made. If fits occur they should be 
watched and the temperature taken ; if there is pyrexia 
preceding the fit it strongly suggests general paralysis, 
especially if the fits are irregular and indefinite, consisting 
simply of twitching of the face or a limb, but not spreading 
in a definite march. As a rule, the Jacksonian epilepsy of 
syphilitic meningitis is preceded or very soon accompanied 
by severe headache, and the fits have a definite onset and 

When the syphilitic meningitis affects the speech centre 
various affections of speech occur, but if these be care¬ 
fully analysed they are seen to be quite different to the 
characters of the speech in general paralysis. It is 
necessary to point this out, for I have in my mind, 
a patient at present in one of the asylums who is 
described as suffering from general paralysis in the case¬ 
book, but who is suffering from typical motor aphasia of 
four years’ duration with some hemiparesis due to vascular 
occlusion. It is only by a better study of the pathology of 
the diseases in question that we can expect medical officers 
to differentiate between coarse lesions and progressive atro¬ 
phic degenerative processes. It is, however, of importance 
that they should do so, both for treatment and also for the 
proper differentiation of true hereditary insanity and non- 
hereditary organic brain disease with mental symptoms. 

In many cases a diagnosis under existing conditions by 
the medical officers is impossible, but I consider that every 
effort should be made by the authorities to make a sharp 
distinction between insanity, which can, and probably will, 
be transmitted, and organic brain disease with mental 
symptoms that probably will not be transmitted. I know 
of no question of more vital importance in asylum statistics. 
The relief expressed by the friends of patients whom I have 
interviewed when I am able to tell them that I do not 


think the mental disease will he transmitted, convinces me 
that with the spread of education the poor will demand what 
is assured to the rich, an answer to the question: “ Is 
this mental affliction likely to affect the children or other 
members of the family?” A correct answer can be given 
only when a correct diagnosis is made and when the statistics 
are based on reliable evidence. 

Early cases of tabes with ocular phenomena can easily 
he mistaken for syphilitic meningitis, e.g., 22 and 27. It is 
yet doubtful whether C is not a case of true syphilitic 
cerebro-spinal meningitis; it is certain that B is tabes. 
Unilateral affection of cranial nerves points strongly to 
syphilis. Ophthalmoplegia interna points rather to tabes 
or dementia paralytica than brain syphilis. The para- 
syphilitic affections are, as a rule, comparatively painless. 
It must, however, be borne in mind that some cases of true 
brain syphilis may be accompanied or followed by the pro¬ 
gressive primary degenerative process, and Minor believes 
that the transitory ocular paralysis met with in tabes and 
general paralysis are true syphilis. I have now seen a few 
cases of cortical epilepsy with progressive dementia and 
paresis in persons having a definite history and well-marked 
evidence of syphilis upon the body and yet not presenting 
the clinical picture of general paralysis. 

The fits had a definite march and many commenced by 
a definite onset like Jacksonian epilepsy, so that it may be 
thought that there is some focal lesion, as in the Cases 
49, 52. At the post-mortem nothing was found in the brain 
to account for the Jacksonian character of the fits. There 
is general atrophy of the convolutions, the ventricles are 
dilated, sometimes granular, the pia arachnoid thickened, 
the perivascular lymphatics are not dilated, the cells are 
not much atrophied, the various layers can be made out 
perfectly and the larger cells show the second and third 
branches of the dendrons and Nissl granules to some extent. 
The glia cells are increased and there is an excess of leuco¬ 
cytes around the vessels. It is a chronic process of diffuse 
encephalitis affecting the central nervous system, probably 
primary atrophy of the finest terminations of the dendrons 



and collaterals of the axons, without acute changes in the 
bodies of the cells and the larger processes. I suppose this 
would be looked upon by some authorities as syphilitic 
general paralysis. Some of these cases in which the fits 
are not of Jacksonian type but resemble idiopathic epilepsy 
may come under the class described by Fournier as post¬ 
syphilitic epilepsy. 

Neurasthenia may arise in the secondary stage partly 
from the direct effect of the toxin upon the system, 
very often due, however, to the depressing influence upon 
the body and mind of a neurotic individual by the con¬ 
sciousness of the nature of his affection and aggravated 
by alarm and fear of the consequences. Too often medical 
men and friends of the patient do not exercise discretion, 
and serious mental symptoms may develop in consequence, 
leading to suicidal and even homicidal tendencies. A 
nervous individual should be cheered up and told that there 
is little fear of his not being cured, it might even be justifi¬ 
able to lead him to believe that you were not at all sure 
of your diagnosis, provided you could thereby keep him 
under treatment. Patients who have had syphilis often 
develop hypochrondriasis and hysteria. They read up or 
hear of possible complications and then imagine they have 
them. One must, however, be always on one’s guard lest 
there is an element of reality in these cases ; e.g., a patient 
was under my care for brain meningitis, from which he made 
a good recovery. He came to me a year later with a slight 
pain in the left side ; beyond that, he had nothing pointing 
to cord disease. I stated to him that I hoped that it was 
nothing more than muscular pain, but he was to come and 
see me again if he was not better. A week later I was 
asked to see him by a practitioner who regarded his case as 
functional. He was paralysed in the lower extremities; it 
had come on somewhat suddenly. Knowing the history of the 
patient, I took him into the hospital, and for the first few 
days he rapidly became worse and lost complete control 
over the bladder and rectum as well as complete loss of 
sensibility below the level of the seventh rib. Under anti¬ 
syphilitic treatment he’made a complete recovery. 


Hysterical paralysis and hystero-epilepsy, according to 
Lang and Fournier, sometimes occur in the secondary stage 
of syphilis and the symptoms disappear under anti-syphilitic 

It will be observed that one case of cerebral syphilis 
was diagnosed on account of the pigmentation of the skin 
as Addison’s disease. The resemblance, however, as I have 
pointed out, was superficial and slight. Symptomatic 
diagnosis is, I admit, all that can be made in many cases, 
but the translation into Greek of a statement which has 
been given in English is a reflection on our ignorance of the 
cause of those conditions which we term mania or melan¬ 
cholia. It is the same in medicine when icterus and ascites 
are diagnosed, or when the diagnosis of hemiplegia satisfies 
the friends who had already informed the doctor that the 
patient was paralysed in one half of his body. There are 
many forms of insanity in which for a long time we shall 
have to be content with “ symptomatic diagnosis,” but of 
all the causes of insanity none writes with such a broad and 
indelible hand as syphilis, and it is for this reason that I 
have endeavoured to study the effects of syphilis, believing 
as I do that it will indicate the way to a better understanding 
of other forms of insanity arising from totally different 
causes but producing often similar symptoms. Moreover, 
the early diagnosis of syphilitic brain disease is of great 
importance, on account of its curability, provided the disease 
is treated before destructive changes have become advanced. 
Destructive changes, however, in the “ silent parts” of the 
brain may proceed to a great extent without producing 
defined symptoms, and the diagnosis of syphilitic brain 
disease which is producing only mental symptoms is of far 
greater difficulty than when there is some definite physical 
symptom such as paralysis of a cranial nerve. Case 44 was 
a typical example of this. 


An analysis of the cases recorded here shows that it 
is impossible to make any statistical statement as regards 
prognosis except in regard to hospital cases, as a very large 



proportion of the asylum cases were diagnosed post mortem 
and therefore had not had the benefit of treatment. Some 
of the patients, however, had been treated in hospitals 
before admission to the asylum and yet had got steadily 
worse. It appears to me that cases of multiple gummata, 
diffuse meningitis and arteritis occurring usually within the 
first few years after infection are especially severe, and 
frequently progress in spite of treatment. Cases 31 and 32, 
however, are instances where treatment in an asylum has 
been followed by decided benefit. 

It would be obviously useless to make up any statistics 
from these cases as regards prognosis, seeing that they 
represent two distinct classes; they only include a few 
selected cases from the asylums, especially the fatal ones. 
Again, although the hospital cases represent nearly all the 
cases which have occurred at Charing Cross Hospital during 
the last few years, it must be borne in mind that, as a rule, 
chronic nervous cases drift eventually into the workhouse 
infirmaries or asylums and die there after a variable time. 
Some of the cases are doubtless cured completely, some 
are cured temporarily, many are left physically incapacitated 
and weak-minded, and in a considerable number the disease 
progresses, frequently in spite of treatment, until, bedridden 
and helpless, they are carried off by some intercurrent 

For reliable statistics we must go abroad, as London, 
with its enormous floating population, special and general 
hospitals, infirmaries and asylums, all independent of one 
another and with little systematic accord, is a most un¬ 
reliable source of information, although there is an unpre¬ 
cedented wealth of material. 

Statistics regarding Prognosis. 



Naunyn. # 




24 (probable). 

Improved .. 



6 * * 






10 (treatment no 

* Eighty-eight cases treated since 1872, in three of which for ovor five years 
no symptoms had occurred. 


The above statistics represent three countries, France, 
Germany, and Scandinavia. Naunyn’s statements are not 
nearly so unfavourable as Hjellmann’s, and I should judge 
would be more in accord with what would be found at our 

One fact stands out in my cases, and that is the bene¬ 
ficial influence of early treatment, and all the writers on 
this Bubject are agreed upon this point. Hjellmann, Lang 
and others (and my experience coincides) believe that these 
nervous affections are more likely to occur when mercurial 
treatment has either been insufficient or not practised. A 
good many of my cases had had no constitutional treatment 
prior to coming under my care and observation. The most 
successful cases were those which pointed to a local gum¬ 
matous process — especially, localised cortical irritation 
causing Jacksonian epilepsy. 

The most unfavourable are those which simulate general 
paralysis, for it indicated universal affection of the brain; 
likewise cases which indicate softening from arterial oc¬ 
clusion are most unfavourable ; probably endarteritis is the 
most dangerous and the most insidious of all forms of cere¬ 
bral syphilis; advanced disease may occur without pro¬ 
ducing any very definite symptoms, perhaps persistent 
headache only, perhaps transitory aphasia, monoplegias or 
hemiplegias following a faint or a fit; if such a case be 
treated at once the prognosis is much better than later, 
when the loss of function has become permanent, for this 
denotes tissue necrosis, and little good can be done towards 
curing a hemiplegia when contracture has occurred. Too 
often a favourable prognosis is given in such cases because 
it is of syphilitic origin, owing to a lack of understanding of 
the pathological process. Nervous tissue once destroyed 
cannot be replaced. Many of the cases show that brain 
syphilis frequently follows a head injury. Thfese cases 
generally responded well to treatment, probably the injury 
caused a local node or gumma, and we know that frequently 
we can see these disappear under treatment in other parts 
of the body. 

Pure basic meningitis does not indicate a bad prognosis, 



neither does participation of a cranial nerve, e.g., motor 
oculi, rather the reverse, for it brings a patient early under 
treatment. Marked choked disc may disappear and restora¬ 
tion of sight may be complete under treatment (Cases 16 
and 17). 

Progressive neuritic atrophy generally ends in blindness. 
Basic meningitis is much more favourable when limited to 
one side. Frequently, however, it is associated with ar¬ 
teritis. The prognosis then is bad because occlusion of 
arteries at the base of the brain may occur and a very small 
patch of softening in the pons or medulla may lead to 
serious paralysis and fatal complications. Acute bulbar 
paralysis is not necessarily fatal, as Case 13 shows. Some¬ 
times bilateral hemiplegia and pseudo-bulbar paralysis 
occurs, and the prognosis is not so bad as in bulbar 

The prognosis of brain syphilis largely depends upon the 
age, habits, life and occupation of the individual. 

All causes which tend to lower the general vitality of the 
tissues of the body or throw stress upon the nervous system 
influence unfavourably the prognosis. I am convinced that 
a most important element in the development of brain 
syphilis are excesses in baccho et venere. An unfavour¬ 
able prognosis should be given when there is reason to 
believe the patient is addicted to drink. Very probably the 
progressive character of the disease in Case 35, in spite of 
treatment, was due to the fact that he was a potman. Age 
is a relative thing, the more worn out a man’s tissues are, 
the more active usually is the syphilitic poison. It attacks 
the locus minoris resistenticc of the individual. Probably, 
therefore, brain syphilis, manifesting itself after 40, is of 
evil omen; not necessarily, however, as Cases 8 and 12 


This resolves itself into two headings. (1) Prophylactic, 
(2) Therapeutic. The prevention of the spread of syphilis 
by legislation is a most difficult problem. In countries 


where the Contagious Diseases Acts are in force, syphilis is 
rife. Evidences, however, among European nations are 
now not wanting to show that civilisation has at last 
awakened to the danger of this widespread disease upon 
men, women and children. An international conference 
meets in Brussels in September to discuss the preven¬ 
tion of syphilis, which is only second to tubercle in its 
disastrous effects upon the human race. All sentimentality 
should be thrown aside and a full consideration of the facts 
discussed, when it is hoped that some solution of the thorny 
problems of remedial legislation may be found. Some time 
ago a commission of enquiry upon leprosy was held in this 
country. I do not believe twenty cases could have been 
collected in London; but here is a contagious disease 
affecting rich and poor, and responsible for a large part of 
the misery and suffering of the race, rendering people in¬ 
capable, by mental and bodily disease, of maintaining them¬ 
selves, and thus being not only a source of danger but of 
expense to the community. If we could get rid of drunken¬ 
ness we should do very much to prevent the spread of 
venereal disease, and the converse is also true. 

The question will sooner or later have to be confronted. 
Shall it be by relying upon education of the masses and 
improvement of the moral instinct—for this we may have to 
wait a long time—or shall it be by some form of remedial 
legislation ? As in tuberculosis, very much real good could 
be done by education. Not nearly so much mischief would 
be done to innocent women and their offspring if it were 
widely known among the lower classes that a wife will 
probably be infected and the offspring also, if she marry 
while the disease is active. 1 Usually the disease is painless, 
and it is often therefore unheeded and not properly treated 
until some severe complication arises which brings the 
sufferer to the hospital. 

Another very important social question is the widespread 
contagion of syphilis in the Army; a very considerable 

1 1 attribute to this fact the relative infrequency of general paralysis 
among women in the upper as compared with the lower classes. 



number of the cases recorded, thirty per cent, of the males 
have been in the services. With the short service system, 
they frequently leave the Army with the effects of recent 
infection upon them, and they sometimes marry and infect 
their wife and offspring. In the statistics {vide Case 57) 
compiled at the asylums they are designated labourers, 
artisans, etc., and therefore there is apparently little 
insanity in the Army; for, of course, general paralysis 
seldom comes on until between thirty and forty, when the 
man has left the Army. I am informed also that when in 
hospital their pay is reduced, consequently they avoid the 
hospital, or get out of it as soon as possible. I have noticed 
that a number of these nervous cases were men who had 
been in the Army, who either had had a very mild attack 
while in the services, or sometimes the infection was looked 
upon as a soft sore and only treated locally for a few weeks, 
or else they have deliberately avoided treatment. This is a 
false economy, for many of those men, in consequence, are 
not only permanently disabled, but come upon the rates for 
a great number of years in consequence of such inadequate 


As a rule I have found the most benefit from mercury 
combined with iodide of potassium. Some authorities 
prefer only the latter in doses of 10 to 30 grains three 
times a day. I generally combine mercurial inunction or 
mercurial injection when it is necessary to get patients 
rapidly under the influence of anti-syphilitic remedies. If 
there is local pain, as in meningitis of the convexity, the 
head may be shaved, and mercurial ointment, combined with 
lanoline, rubbed in over the painful part as well as into the 
body. Should the patient be unable to retain medicine and 
food on the stomach owing to vomiting, iodide may be given 
in the nutrient enemata. I usually have found 10 to 30 
grains of iodide, combined sometimes with liq. hyd. per- 
chlor, 1 to 2 drms.; spirit ammon. arom., 20 m., and tinct. 
cinchona, 1 drm.; aq. 1 oz. T.D.S.P.C. useful for out- 


patient practice. For inunction I use ung. hyd., 1 drm.; 
lanolin, 1 drm.; bis. die. rubbed into the back, thighs and 
various parts of the body until the gums commence to be 
spongy. Care should be taken to tell the patient to clean 
the teeth after each meal, and a mouth wash of chlorate of 
potash may be ordered. Many patients’ gums are touched 
long before they have had efficient mercurial treatment, 
owing to neglect of these precautions. 

Direct injection of mercurial preparations into the veins 
I have not tried, as I have obtained good effects by the other 
means related. 

As a rule, good effects will begin to show themselves in 
the first week or two, but the treatment should be continued 
for months: for if it does not at first lead to visible im¬ 
provement, it may prevent the extension of the disease. I 
generally keep my patients for months, and even years, on 
moderate doses of iodide, occasionally combined with mer¬ 
cury, according to whether it is an early case or late case, 
after infection; and I consider that those who persistently 
followed the course of treatment have yielded much more 
satisfactory results, in having had no return of symptoms, 
than those who neglected to attend. It is of great im¬ 
portance to point out to the patients the desirability of 
leading a sober and steady life, and also it is the duty of the 
medical man, and I consider it a most important element in 
the treatment, to cheer up the patient by encouraging him 
to believe that he will recover and be able to resume his 

Case 1 .—Syphilitic arteritis, followed by softening, transitory 
paralysis. Epilepsy. Brain disease eight years after infection. 

W. W., aged 32, male, farm bailiff; married eight years; four 
children. Contracted syphilis at 13. Treated for two years. 
Had sore throat and rash. Children all healthy. Habits 
temperate. Six years ago while at work he had a fit and lost 
consciousness. He had previously suffered from loss of memory of 
words, knowing what things were but he was unable to name them. 



After the fit his speech became thick, then he had several more 
fits, after which he had paresis of the right limbs and his face 
was slightly drawn. He suffered about this time with headache, 
which was worse at night. He has now no paralysis or aphasia, 
but for the last five years he has suffered with fits. Sometimes 
three or four a day, sometimes only one or two a week. 

Description of fit by his wife.—Both cheeks became flushed. 
He complains of dimness of sight for some hours before. The 
fits begin by conjugate deviation of the head and eyes to the left. 
He then makes a gurgling in the throat, followed by tonic spasm 
in arms and legs. The arms are extended, the fingers clenched 
in the palm. No clonic spasms follow. He then breathes 

Case 2 .—Syphilitic arteritis, thrombosis, hemiplegia, softening, 
epileptiform convulsions. Brain disease eighteen years after 

F. C., male, aged 46. Admitted into Claybury, January, 1895. 
Deaf in both ears. Syphilis at 20. Scars on legs, scars of rash 
over forehead very severe. History of heavy drinking; eight 
years ago paralysed on right side. There is now weak grasp on 
the right side and numbness ; right facial paresis. Spastic gait. 
Foot clonus on both sides. Almost stone deaf. Admitted because 
he had epileptic fits. Says that if he drank heavily fits were 
sure to follow. For the last two years in the asylum he has had 
no fits. 

Case 3 .—Married woman, probable infection after marriage, 
hisUrry of two stillborn children, then a child which died at 
three months. Admitted for fits and mental depression. 
Probably brain symptoms first manifested seventeen years 
after infection. History of alcoholism. No history of epilepsy 
or fits in family. 

C. T., aged 36, married at the age of 19. First baby stillborn, 
six months; second stillborn, seven months. Third died at three 
months with convulsions. Six children since, all alive. No 
history of epilepsy, fits, or insanity in family. One year ago she 
attended a hospital for a painful swelling over the right fronto¬ 
temporal region. She took medicine for six weeks. As it got 
better, neglected to go any more to the hospital. In January she 


commenced to have fits. She does not know that she had any 
warning. The first fit she had, occurred when she was going 
from one room to the other. She fell down and lay unconscious 
for some time. She did not bite her tongue or pass water. She 
has suffered with severe headache, worse at night. When ad¬ 
mitted, she was in a stuporose condition. The nurse says that 
previous to her fits she becomes dull and somnolent. She does 
not bite her tongue in the fit, but passes water. 

Patient is tall and well nourished. Answers questions in¬ 
telligently and without any noticeable affection of speech beyond 
a slight hesitation, which might well be accounted for by a little 
nervousness. The tongue is protruded without jerkiness or 
tremor. There is no tremor of lips when the teeth are exposed 
and no tremor of the fingers. The knee-jerks are exaggerated 
and there is a fair wrist tap contraction. The pupils dilate with 
atropine ; they were unequal. The left disc is hazy at the edges, 
as if there might have been a little optic neuritis. The right is 
normal. She has suffered with vomiting and headache since she 
has been in the asylum. During the first month she had twenty- 
eight fits, the second month eighteen, and none since. Under 
treatment she recovered considerably, and was discharged ten 
months after admission. 

Case 4.— Soldier infected with syphilis when 22, syphilitic brain 
disease three years after infection. Commenced with sudden 
onset. Left hemiplegia and lefi ophthalmoplegia externa and 
interna. Threatened to kill his wife, admitted to Claybury 

M. C., aged 29. Joined the army when he was 20, remained 
in the service for three years, when he took his discharge, aged 
23. One year previous to discharge he contracted syphilis. Hard 
sore, rash, sore throat. Was treated in the hospital for it. For 
two years after his discharge he worked as a bricklayer’s labourer. 
During this time he was a teetotaler; married, had three children, 
the first one dead, no miscarriages. Three years after he had 
syphilis he had what he calls a fit, followed by ophthalmoplegia 
externa and interna, accompanied by left hemiparesis. He was 
treated with iodide and bromide in Higbgate Infirmary. There 
is no evidence of hemiplegia now. He was sent to the asylum 
because he threatened to kill his wife. There is complete 
paralysis of the third nerve of the left eye. No scars or signs of 
syphilis on the body. 


Case 5.— Specific basic meningitis, occurring in a man aged 32 ; 
history of syphilitic affection six years ago wtien m tne army. 
Sore throat, no rash, very mild attach. Married five years, 
one child four years old. First cerebral symptoms occurred 
five years ago, therefore one year after infection, when he had 
iritis, squint, and double vision. 

T. M., aged 32, attendant, complained of headache when the 
least fatigued for some time past, but not until a fortnight ago 
did it affect his sleep; then it would wake him up about three 
o’clock and last till six o’clock in the morning. The pain was 
referred to the frontal region. Deep-seated neuralgic, not relieved 
by any medicines; but for the pain, he felt quite himself. The 
headache had lasted about a fortnight when he was seized with 
vomiting, giddiness, and stiffness in the neck. He became partly 
unconscious, no twitchings. Consciousness returned for a few 
hours; he was again attacked, and he remained unconscious for 
twelve hours. 

Present state. —There are no scars on the body but there 
are posterior synechise in the left eye. Conjunctival reflexes 
present. He is unable to see objects held in front of him. Is 
able to answer questions, but readily dozes off. He has tender¬ 
ness on percussion over the whole frontal and temporal regions. 
He feels perfectly all over his body. He will put out his tongue 
or show his teeth when told to do so. Knee-jerks absent. 
Plantar, abdominal, and cremasteric reflexes present. He has 
constipation, but no difficulty with his water. Pupils do not 
react to light. There is well-marked optic neuritis on both 
sides. No tache cerebrale, no affection of speech, no affection 
of hearing, no coarse paralysis, can swallow fluid food without 
difficulty. Pulse 72 small. Temperature: slight pyrexia for 
a few days, then became normal. The attendant states that 
he always is thirsty and drinks very large quantities. Poly¬ 
dipsia and polyuria. — The above notes were made by me 
when I first saw him. Evidently the disease had been in 
existence for some time, dating back probably weeks or even 
months, when the headache was first noticed. I recommended 
large doses of iodide of potassium and mercurial inunction. 
He had several left-sided fits, but gradually improved under 
treatment, with the exception of his eyesight, for double optic 
atrophy ensued. A month later, when I saw him, I made the 
following note:—Patient is sitting up in a chair, quite blind. 
Slight ptosis of left eye. Both pupils inactive to light and to 
accommodation. Knee-jerks still absent. Temperature sub- 


normal. No pains in legs. Constipation. Wet and dirty. Speech 
unaffected. Memory very bad. Tongue slightly tremulous. No 
delusions or halluciations. Feels drowsy at times. Can stand 
and walk. No unsteadiness of position. Knee-jerks present 
when he was pulling with hands. Naso-labial fold of left side 
less marked. Eats ravenously. A week later: There are no knee- 
jerks even when pulling with hands. Walks fairly well. F.W.M. 

Case 6.—Male, aged 34. Syphilitic arteritis, thrombosis, cerebral 
softening. Right hemiplegia eight years after infection. 
Treated thoroughly. Development of unilateral right-sided 
epileptiform convulsions. Loss of memory and dementia. 

Case 7.— Gummatous meningitis, affecting motor area of right 
hemisphere twenty-three years after infection. History of 
injury, 400 Jacksonian epileptiform fits. Cured by vigorous 
anti-syphilitic treatment three weeks after admission to 
Charing Cross Hospital. 

W.S., policeman, aged 46, syphilitic infection twenty-three 
years previously. No history of fits in family, nor any nervous 
disease. Has had peripheral facial paralysis from infancy. While 
on duty he was taken in a fit, lost consciousness, brought to the 
hospital by a comrade. During the first nine days he was in the 
hospital, he had over 400 fits. Each fit lasted altogether about 
two minutes. He does not lose consciousness, but is only semi¬ 
conscious. The fit commences with conjugate deviation of the 
head and eyes upwards and to the left, followed almost immediately 
by twitching of the left side of the face, clonic spasms of the arm, 
which is in a semi-flexed position, and quite rigid. There was 
slight contraction of the right arm at the shoulder and both legs. 
Between the fits the head and eyes deviated to the right (paralytic 
exhaustion). Left arm is weaker than right. Legs: no obvious 
paralysis or paresis. Reflexes, both knee-jerks slightly exaggerated. 
Left ankle clonus more than right. Superficial plantar, left 
absent, right present. Memory good. Treated at first with 
chloral hydrate and bromide. I was asked to see him, expressed 
the opinion that it was syphilitic gumma, recommended mercury 
and iodide. He was put on hypodermic injections of one-eighth 
grain hydrarg. perchlor. every day at first and every other day 
afterwards, and large doses of iodide. A blister was placed over 
the shaved scalp, corresponding to the lower part of the right 
motor area. From this time the fits began to diminish, and a few 



days later ceased. He was discharged three weeks after admission ; 
subsequently attended with my out-patients. He was able to 
earn his living as a caretaker. 

Case 8 .—Gummatous meningitis of the left parieto-occipital region. 
Syphilitic infection twenty years before, untreated. Severe 
headache. History of injury. Visual sensations like megrim. 
Cured by anti-syphilitic remedies. 

J. J., aged 89, clerk, came to me suffering with severe pain in 
the head, which he thought was neuralgia at first; no relief 
obtained by the ordinary remedies. There is a tender area the 
size of half-a-crown over the left occipital parietal junction. He 
has no fits, but curious visual sensations, which correspond to 
teichopsia. Hearing is perfect, optic discs normal on both sides. 
No sickness. The symptoms were very much like megrim, but 
the history of infection twenty years before, which he at first 
totally denied, the local tenderness, together with the continuous 
headache, suggested the advisability of anti-syphilitic treatment, 
although there were no signs of syphilitic residua on the body. 
This was adopted, and he made a perfect recovery. 

Another very similar case to this occurred in my practice, 
in which there was a history of injury, but the patient denied 
syphilis. He was, however, completely cured by anti-syphilitic 

Case 9 .—Gumma involving the right third nerve. 

J. L., aged 49, coachman. Syphilis twenty years ago. Blow 
over right supra-orbital region four years ago. Alcoholic history. 
No neuropathic history in family. Admitted under my care at 
Charing Cross Hospital. 

Symptoms .—Paralysis of third nerve on right side, diplopia, 
ptosis, internal and external ophthalmoplegia. Bight hemiparesis. 
Slight thickness of utterance. Knee-jerks absent, plantar reflexes 
present. Bight radial reflex exaggerated. He was put on mercury 
and iodide. After a few days in the hospital he became delirious 
and suffered with frequent vomiting. Slight optic neuritis in the 
right eye. He improved rapidly under treatment and was dis¬ 
charged six weeks after admission almost well. He continued 
as an out-patient, and has now so far recovered that he can 
resume work. 


Case 10.— Syphilitic basic meningitis six months after infection, 
followed seven months later by left hemiplegia and neuritis. 

B. EL, aged 29, stableman. Sent to Charing Cross Hospital 
by Dr. Maude. Contracted syphilis in July, 1897. Was treated 
regularly for several months at Guy’s. He had secondary 
symptoms two or three months after. Sore throat. Left off the 
medicine, thinking he was well. Fresh throat trouble commenced 
in January, 1898. In February, 1898, he suffered with severe 
headache, and Dr. Maude, under whose care he came, states that 
there was slight irregular pyrexia, very slow pulse and marked 
tenderness over the frontal region. He had no squint or vomiting. 
Basic meningitis was diagnosed, and for some months he was 
kept on mercury and iodide. In the beginning of August, 1898, 
he complained of numbness in the left hand and arm, then a few 
days after, almost suddenly, he fell down in a fit, but did not lose 
consciousness completely. He was merely dazed. This left him 
with left hemiplegia and dysarthria. Admitted to Charing Cross 

Condition on admission. —Paralysis of lower part of face on 
left side ; he can whistle, hut cannot wink the right eye. Complete 
paralysis of the left arm, weakness of left leg. Speech a little 
indistinct and slow, no opthalmoplegia. Sensation unimpaired. 
No optic neuritis. Temperature normal. Inguinal, cervical, and 
axillary glands all enlarged. Frontal headache, no vomiting. No 
neuropathic history in family. Treated with mercurial inunction 
and iodide. A little later he began to complain of tenderness on 
pressure in the limbs. The pain in the left arm is very severe and 
prevents sleep. There is tenderness on pressure in both lower 
limbs, with weakness but not paralysis. Superficial reflexes pre¬ 
sent. Knee-jerks absent. Muscles flabby and wasted. Electrical 
reactions. All the muscles of both arms react normally to galvan¬ 
ism and faradism, except the interossei, which react but feebly to 
faradism, and in the left hand the reaction to galvanism shows 
K.C.C.=A.C.C. Legs: the muscles all react normally except the 
extensores longi digitorum, which do not respond to either current. 
Complains of stiffness in the neck and back. He was dull and con¬ 
fused, but no obtrusive mental symptoms presented themselves. 
His symptoms at first increased, and the pain in all his limbs, 
but especially of the left arm were very severe, and repeated 
morphia injections and antipyrin had to be administered for relief 
of his suffering. 

Diagnosis. —Endarteritis. Softening of the motor region of 
the right hemisphere. Cerebro-spinal meningitis. 




Eventually, under anti-syphilitic treatment, he made a very 
good recovery, and on December 10 he was looking well, and 
there was only paresis in the left hand and face. He is now an 
out-patient, and I shall keep him under treatment for a year at 

January, 1899. Patient has now no coarse paralysis and very 
little obvious paresis; but, though he has gained weight, he is slow 
in his understanding and responding to questions ; there is loss of 
expression in the face, and his speech is just a trifle thick. 

April. Patient remains in about the same condition and his 
general health is good. 

Case 11.— Syphilitic basic and spinal meningitis. A combined 
sclerosis within four years of infection. Extension of menin¬ 
gitis to the convexity affecting the left motor area. 

M. M., formerly in the army, aged 29, van driver, admitted 
into Charing Cross hospital on July 13, 1897, under Dr. Aber¬ 
crombie for weakness of legs. Contracted syphilis while in the 
army four years ago. Treated at Guy’s for eighteen months. 

History of present illness. —While driving his van he became 
giddy, a ringing in his ears occurred, he lost consciousness and 
fell off his van. He remembers nothing until he found himself 
at home in bed. 

Condition on admission. —Paresis of all the limbs. Deep re¬ 
flexes exaggerated. No foot clonus, paralysis of left external 
rectus. Pupils equal, react to light and to accommodation. No 
impairment of sensation. He suffers with fits which begin with 
clonic spasm in the right leg, spreading to other limbs and face, 
followed by severe headache. Temperature normal. He was 
.put on ten-grain doses of iodide of potassium, but the fits 
persisted for some time; eventually he became better. Re-ad- 
mitted June 6, 1898. He now complains of pain in the back of 
the head and neck and across the eyes, which is worse at night, 
preventing him from sleeping. The only evidence of mental 
affection he has, is a loss of memory. His gait is staggering, 
crossing his legs and bringing his feet heavily to the ground. If 
he closes his eyes while standing, he sways to and fro, and falls. 
Marked tremor of the arms and legs when he attempts to move 
them. There is some atrophy and marked loss of power in the 
muscles of the arms and legs, but the electrical reactions are 
normal. There is no facial paralysis and his speech is unim¬ 
paired. Tactile sensation is diminished in the arms and legs. 


Knee-jerks exaggerated on both sides and ankle clonus can be 
obtained. Superficial reflexes are absent. There is internal 
strabismus and almost entire loss of vision of the right eye. 
With the left eye closed there is no reaction to light or accom¬ 
modation. Optic neuritis well marked on the right side and to 
some extent on the left. The patient had daily fits commencing 
in the right foot and spreading to the other limbs and face, with 
conjugate deviation of the head and eyes to the right. A little 
later he had severe pain in the left temporal region. Made a 
partial recovery upon mercury and iodide. 

Case 12. —Basic gumma. Protrusion of the right eyeball twenty- 
five years after infection. Complete cure. 

W. B., aged 45, married eighteen years, no children. Nothing 
in family history. Present illness commenced with weakness. 
Syphilis twenty-five years ago. Admitted under my care in 
Charing Cross Hospital on April 23, 1898. Severe headache 
began two months ago, at first frontal, only gradually extended 
to right circumocular region. Pain continuous, dull, aching, 
sometimes throbbing. The right eye became prominent, he 
suffered with squint and double vision. About three weeks ago 
vomiting began, which was very severe. He also complained of 
frequent micturition, every half hour during the day, and several 
times during the night. He passed a large amount of urine and 
there was a corresponding thirst. 

Present condition. —Well built, weight 13 st. 4 lbs., pulse 48, 
irregular, fairly compressible, respirations 14, urine normal colour, 
acid, 1,020, no albumen, no sugar. Mental state good. Eyes: 
proptosis of the right eye, oedema of the lower eyelid. Pupils, 
right slightly larger than left, both react to light. Movements, 
up and down normal, lateral movements quite lost. Double 
optic neuritis, retinal veins enlarged. Blurring of the margin of 
both discs. Vision $ both sides. No facial paralysis. Heart 
and lungs normal. Scar on glans penis. Tissue paper scars on 
legs and chest. Reflexes normal. There was considerable limit¬ 
ation of the field of vision to white, red, and green in the 
right eye. 

Case 13.— Syphilitic arteritis, thrombosis, six months after infec¬ 
tion. Sudden paralysis of the pharynx, soft palate and vocal 
cord of the left side, follotved by left hemiplegia. 

W. R., aged 38, commercial traveller, contracted syphilis in 
Japan. Six months later, while playing the piano and singing, 



felt faint and giddy, and, trying to drink a glass of water, found 
that he was unable to swallow it, the fluid regurgitating through 
bis nose. This was followed the next day by weakness and 
paralysis of his left leg, left arm and left side of the face. For a 
month he had to be fed with a tube. He was treated by mer¬ 
curial inunction and made a good recovery, as he was able to 
swallow after a month and to speak. He was sent to me on bis 
return from Japan, and he now presents the following symptoms: 
There is well marked late spasm of the facial muscles of the left 
paralysed side owing to the great affection of the lower facial 
muscles. The tongue protrudes slightly to the left. The left 
soft palate moves less freely than the right, but there is no evident 
paresis now of the left vocal cord. The patient is able to close 
both his eyes tight and to wrinkle his forehead on both sides, but 
there is a marked difference between tbe two sides, the wrinkles 
on the left side being much less obvious. His speech is slow and 
somewhat scanning. He has considerable weakness in the legs 
but no wasting of the muscles. The gait is spastic and there is 
rigidity and slight ankle clonus, and exaggerated knee-jerks on 
both sides. The wrist tap contraction can be obtained on both 
sides. Pupils equal and react to light and to accommodation. 
Patient improved considerably under my care, and two years later 
he came and told me that he was able to earn his living as a 
billiard marker. He has no mental symptoms beyond weakness 
of memory. 

Case 14.— Paresis of left vocal cord of left side of soft palate. 
Pain in head. Numbness of left arm and fingers and some 
weakness occurring in a young married woman, who had been 
suffering from symptoms probably secondary syphilis. 

Mrs. R., aged 31. Sent to me at Charing Cross Hospital as 
a case of diphtheritic paralysis. Patient is married and has four 
children all living. She was unable to tell me any information 
respecting the origin of her illness. She complains of severe 
headache in the morning which passes off after a little while. 
The voice has a nasal character and fluids regurgitate through 
the nose. She complains of weakness and numbness of the left 
arm and fingers. Knee-jerks are normal, or if anything a little 
exaggerated on the left side. Her hearing is impaired on the 
left side. Her hair has been falling out. Examination showed 
paralysis of soft palate and left vocal cord. Pupils equal, react 
to light and to accommodation. There is a squamous • papular 
eruption on the chest. Patient was put on anti-syphilitic treat- 


tuenfc and rapidly improved. Six months before she came 
to the hospital she had sore throat; none of her children 
had been affected. The question of diagnosis was whether it 
was syphilis or diphtheria. Nothing in the oase suggested 
diphtheria except the nasal speech. The unilateral character of 
the paralysis, the knee-jerks being present and the absence of 
paralysis of accommodation all pointed against diphtheria. Pain 
in the head following sore throat, hair falling out, and the 
existence of a pretty characteristic rash, together with the benefit 
resulting from treatment, makes it very probable that it was 
syphilis, although no history could be obtained of infection. 

Case 15.— Syphilitic basic meningitis and arteritis two years after 
infection, right hemiparesis, enophthalmos and hemiancesthesia 
over the distribution of the fifth nerve. 

G. H., aged 31, labourer. Contracted syphilis and neglected 
treatment. Two years after infeotion he found himself one night 
holding on to the bedstead, feeling and suffering from numbness 
on the right side. He went to the doctor, who later on sent 
him to me. He was treated for some time with anti-syphilitic 
remedies. On examination I found briefly the following facts : — 
He had weakness in the right arm and the right leg; slight loss 
of expression on the right side of his face, paresis of the soft 
palate on the right side, and of the right vocal cord. He had no 
paralysis of masseter and temporal muscles. The tongue deviated 
slightly to the right. The most noticeable symptom, however, 
was in the appearance of the two eyes; at first one would think 
there was slight ptosis. There is, however, no paresis of the 
ocular muscles; the pupils are equal and react to light and to 
accommodation. Comparison with a photograph before the 
patient's illness shows a condition of enophthalmos of the right 
eye. The cornea is insensitive, and there was some conjunctivitis 
which was cured with boracic acid lotion. Pricking with a 
needle all over the distribution of the branches of the fifth nerve, 
on the right side, was recognized only as a touch. There was 
dulness of perception of heat, oold and touch on the right side 
as compared with the left; it is the same with the mucous 
membrane of the mouth, the lips, and the tongue. Taste on the 
right side of the tongue is impaired. He oomplains of a stiffness 
of the muscles of the face on the right side, and there is a loss of 
expression. The giddiness, with tendency to fall to the left side, 
which he had at first, is now passing oft The case was shown in 



conjunction with Mr. Treacher Collins at the Ophthalmological 
Society; the notes of the case are published in the proceedings. 
The points of interest in this case are the nature of the lesion 
and the condition of enophthalmos. Since the onset was sudden 
arterial occlusion is probable, and this may have been associated 
with a gumma involving the right fifth nerve. The condition of 
enophthalmos was probably not due to paresis of Muller’s 
muscle, which is said to be supplied by the sympathetic; for, 
at the suggestion of Mr. Nettleship, I put cocaine in the eye 
and found the pupil dilated. 

Case 16.— The following two cases are of interest from the fact 
that two brothers, aged 31 and 32 respectively, were affected 
with gumma cerebri and symptoms pointing to tumour. Both 
made a recovery under treatment. Both brothers had been 

M. G., aged 31, drayman, formerly a soldier. Admitted into 
Charing Cross Hospital with pains in the head. Two years ago 
attended Ophthalmic Hospital for “ blight in the eye.” 

Condition. —Ptosis of left eyelid, optic neuritis, vomiting, severe 
headache, especially on the left 6ide. Said to have had an injury 
where the pain is most intense. He lies in almost a semi-comatose 
condition, from which he is roused with difficulty to answer ques¬ 
tions, which he does in a rambling, unintelligent manner. Breath 
very fetid. Face flushed. Pupils dilated and unequal, the right 
being the larger. Voluntary movement and respiration seem 
unimpaired. Passes motions and water in the bed. Temperature 
generally subnormal. Extremities cold. Knee-jerks present. 
Pulse 64, regular. Came under my care when his brother was 
admitted into the hospital, and he was immediately put upon 
large doses of iodide and mercurial inunction. Discharged well 
enough to resume work at the end of two months, but died six 
months later of pneumonia. 

Case 17. 

G. G., aged 32, carman. Admitted into Charing Cross Hos¬ 
pital for pains in the head and vomiting. Syphilis fifteen years 
ago at the age of 17, for which he was inadequately treated. 
Contracted it while in the army. He only admitted venereal 
infection after I had pointed out the serious results of not speak¬ 
ing the truth. 

Condition on admission. —Severe headache over the right tem¬ 
poral region and forehead, awakening him periodically about four 


o’clock in the morning. Three days previous to admission he was 
seized with a fit, followed by weakness of the left arm and left 
leg. Vomiting without relation to food. Pupils: right some, 
what larger than left, and does not react to light. Optic neuritis 
on the right side. Tenderness on percussion over the right 
fronto-temporal region. He made a rapid recovery under treat¬ 
ment. The patient remained well for two years, but neglected 
my advice to attend regularly the out-patient department. His 
wife came and said that he was again affected ; he was admitted 
to the hospital with left hemiplegia and some thickness of speech. 
Upon anti-syphilitic treatment he improved somewhat, and was 
sent to the convalescent home; but I am afraid he will be perma¬ 
nently incapacitated. 

The interest in these cases lies in the fact that two brothers 
who had syphilis developed almost identical symptoms at almost 
the same age. It is presumed, although the notes do not state 
it, that M. G. suffered from syphilis, by the symptoms and from 
the fact that he recovered so rapidly under the anti-syphilitic 

Case 18.— Syphilitic arteritis, thrombosis, left hemiplegia fifteen 
months after infection. Treatment one month. Occupation, 
seaman in Royal Navy. 

W. T., aged 30, occupation, seaman, Royal Navy. Paralysis 
of left side. Defective memory, thickness of speech. Fifteen 
months before paralysis set in, contracted syphilis. Treated for 
one month at Chatham Naval Hospital, then went to sea, 
when secondary symptoms presented themselves. Sore throat, 
rash, iritis. Onset of paralysis sudden. 

Case 19.— Syphilitic cerebrospinal meningitis, ( probable ) alco¬ 
holism. Infection two years previous to onset of symptoms. 
Occupation, soldier. Three attacks. In last attack treated 
at Charing Cross Hospital. Great improvement upon anti¬ 
syphilitic remedies. 

A. F., aged 32, retired soldier. Admitted into Charing Cross 
Hospital on May 9, 1896. Discharged on July 15,1896. Result, 
greatly improved. He had syphilis two years previous to his first 

Original attack, May, 1894.—Pains in the head, back and 
limbs. Vomiting and diarrhoea. No paralysis. Subsequently 
sleeplessness. Morning votniting. Pains in head and back and 
down right arm and leg. 



Next attack, September, 1895.—Pain in right arm and leg, 
back and head. Vomited blood. Complete paralysis for three 
days. Numbness in left arm and left leg. Sleeplessness and 
diarrhoea. Subsequent partial recovery, then rapid wasting of 
muscles of right arm and right leg. Complete recovery in left 
arm and left leg. Calf muscles of left leg begin to waste. 
Bight foot drop. Continued wasting in both legs and in right 

Third attack .—Pain in head; vomiting. Shooting pains in 
left leg and both arms. Vomited blood; diarrhoea. Admitted 
for pain in head, chest, back, legs and arms, and also for continued 

Present illness .—Patient says he was perfectly well up to the 
month of May, 1894, when he had sunstroke in Egypt. He was 
drilling his company one day, when he felt pain in the back of his 
head and became almost immediately unconscious, in which state 
he remained for twenty-four hours. He was taken to Hospital 
Camp and laid down. On recovering consciousness be got up 
and walked for a quarter of an hour. At the end of this time he 
fell down and again became unconscious. This time he remained 
for fourteen hours. On recovering consciousness again, he felt 
pain in the head, back and limbs, and was violently sick. The 
vomiting occurred many times during the day, and he also suffered 
from diarrhoea. There was no paralysis. The above symptoms 
confined him to bed for one month, at the end of which time he 
was invalided home. On the voyage home he suffered from 
sleeplessness, continual vomiting and pains in the head, back, 
right leg and right arm. He went to Haslar Hospital for six 
months. On leaving that institution, he noticed that the vomiting, 
which still continued, used to occur in the mornings, immediately 
upon getting up. He then went on six months’ sick leave, after 
which he got his discharge from the service. The morning sick¬ 
ness has continued more or less ever since. He also used to 
suffer from pains in the head, and noticed that his right arm and 
leg got thinner. Beyond this he felt nothing more until nine 
months ago. 

In September, 1895, he was residing in Dublin, studying for 
an engineer’s examination. One day, while at work, he felt a 
sudden pain in his head. He rose from his seat and walked up 
and down the room for a quarter of an hour. The pain continued, 
however, and he finally fell forward on his face and bands and 
became unconscious. According to information he afterwards 
obtained from his friends, he vomited, frothed at the mouth and 
brought up blood. On recovering consciousness, he felt pain in 


the right arm, right leg, back and head. The vomiting continued, 
and he found be was unable to move, not being able even to turn 
in bed for three days. He felt a numbness in the left arm and 
left leg. He also suffered from sleeplessness and diarrhoea. The 
above condition of affairs lasted three days, when he found that 
the numbness in the left leg and left arm had gone and he could 
move them perfectly well. As regards the right side, the pain 
still continued in the arm and leg, but he could move them a 
little. The next thing he noticed was that the muscles of his 
right arm and leg were wasting more rapidly than before, and 
that the weakness was increasing in them. The left leg and left 
arm appeared all right during this time. Patient was confined to 
bed for four months after this attack. At the end of two months 
(November, 1895) he noticed that the calf muscles of his left leg 
had begun to waste, also that his right foot had begun to drop. 
At the end of four months the patient went away for a month, 
during which time he managed to get about on crutches. On 
returning home he commenced to study again, but he was unable 
to continue doing so. He travelled about to different places for 
the benefit of his health, and during this time he felt a good deal 
better. He noticed, however, that the wasting still continued in 
both legs and also in the right arm. 

Patient continued in this condition up to Tuesday, May 5th, 
1896, on which day he experienced severe pain in the head, 
and commenced to vomit. Towards evening he felt pain in the 
head, abdomen, and back. The vomiting continued until the 
next morning, when he felt shooting pains in the left leg and 
both arms. These were worse on the left side. The pains in his 
head had become more severe also, so much so that he could not 
bear anyone to touch his head. Last Saturday he felt very ill 
indeed, and vomited blood which was dark and congealed. He 
had pain all over his body and suffered from diarrhoea. Patient 
has had marked and persistent headache ever sinoe his first 
attack in May, 1894. 

Heredity .—Parents both alive and well. Brothers, twenty 
(patient himself is one of triplets); sisters (four) are well. Children, 
seven; five boys and two girls. All enjoy the best of health. 
One child died when three weeks old. Cause of death unknown. 

Past personal history .—He had a sore on his penis four years 
ago. Did not notice any rash or sore throat afterwards. No 
history of alcoholism. Suffered from ague in India, but has had 
no other illness. It may be mentioned that it was subsequently 
ascertained that few of his statements were reliable; e.g., he said 
that he had the V.C. 



Condition on admission .—There is marked wasting of the 
muscles of the right arm and right leg. Hypothenar and thenar 
eminences of the right hand no longer exist as such. The right 
leg is kept in a condition of semi-flexion and rotation out. Foot 
drop is present. On the left side there appears also some wasting 
of the muscles of the limbs. Foot drop is present to a more 
marked degree on this side, and there is some displacement of 
the tarsal bones dorsalwards. In the left eye there is an internal 
squint. Patient cannot lift either of his legs up from the bed. 
He can raise his arms easily above his head. In the right arm 
the power of extension is much weaker than the power of flexion, 
and there is more loss of power in the limbs of tbe right side 
than of the left. Patient cannot flex either of his ankles. Fibrillar 
twitchings are present, both in the arms and legs. He has 
paralysis of the left external rectus. Says he notices that bis 
speech has become slightly altered in the last few days. He says 
his tongue feels flabby and too big for his mouth. 

Sensation .—There is hyperesthesia all over the body and 
head, but this is more marked on the left side than on the right. 
The gums are very sore. No alteration of sensibility to heat or 
cold. There is tenderness of the muscles on pressure both of 
the legs and arms, but this is more marked on the left side. 
There is pain in the left leg. No anaesthesia to touch, heat, or 
cold anywhere. 

Reflexes. —Superficial, plantar present on both sides. Deep, 
left knee-jerk exaggerated. Reflexes of arm exaggerated. 

Nutrition .—The muscles of the left arm and left leg feel very 
flabby. There is marked wasting of the muscles of the right 
arm and right leg. There appear to be no trophic changes in the 
skin. There is an abundance of soft downy light coloured hair 
on both legs. 

Visceral .—Patient vomits continually. He can keep nothing 
down but brandy. He has had the catheter passed four times 
since admission. He has a stricture. He has incontinence of 

Electrical .—The limbs are so tender and hyperaesthetic tbat 
he would not allow the muscles to be tested, although an en¬ 
deavour was made to do so. 

Mental State. —Unaltered. 

May 13.—Patient has shooting pains in the left arm to-day, 
with tenderness of muscles on pressure, together with hyper¬ 
esthesia. The eyes were examined by Dr. Mott. Nothing was 
found except that the discs were redder than normal, and there 
was some swelling. Patient is having liq. morph, acetat. iq ii., 


liq. atrophinsB salph. rq i. injected every night. He does not 
sleep well. He passes his urine without the use of a catheter 

May 14.—The pains in the left arm are worse this morning. 
The muscles are very tender on pressure, and there is hyper¬ 
esthesia. Patient has intense headache. Finds he cannot talk 
as well as he could on admission. Slept fairly well last night. 
Suffers continually from twitching of the muscles of the legs and 
arms. Is now having ung. hydrarg. rubbed into the abdominal 
wall, and is taking (at Dr. Mott’s suggestion) pot. iod. 30 

May 15.—Did not sleep well last night. The pain in the left 
arm is more severe this morning and he complains also of pain in 
his head and back, chest and down the right side. He finds that 
he has greater difficulty in talking than he had yesterday. The 
twitching of the muscles continues. 

Urine .—He is passing 20 ozs. per day. Acid, specific gravity, 
1,030. No albumen. Vomits everything taken, including the 
potassium iodide mixture. 

May 16.—Patient has had 3 ozs. of Valentine’s meat extract 
with brandy, which he managed to keep down. He has vomited 
very little since 8 a.m. About 1 a.m. his breathing became very 
rapid and he became cyanosed. Pulse 88. Respirations 32. 

Had an enema of 2 ozs. of glycerine this morning. He can 
hardly move his right arm on aocount of the pain in it this 
morning. His power of speech is also diminished. Vomiting as 
bad as ever. 

May 18.—Patient is now bringing up a large quantity of dark 
chocolate-coloured vomit. He is unable to keep the meat extract 
down now. Passed a very bad night last night. His hands are 
very blue. Speech about the same. Left arm continues in the 
same condition. Is taking 6 ozs. of brandy daily, but says that 
sometimes he cannot even keep this down. Is taking nutrient 
enemata of milk and beef-tea. 

Vomit .—Dark green-coloured fluid. Acid reaction contains a 
trace of bile. No torulse or sarcinm, or anything noteworthy 
found on microscopical examination. 

May 19.—The vomiting still continues. The left leg is 
exceedingly hyperaesthetic this morning. The left arm still 
remains very tender on pressure. He complains of buzzing in 
his ears. He is taking 8 ozs. of brandy. Had some custard 
yesterday and managed to keep this down. 

May 20.—Patient still vomits a very light green fluid. He 
had three pints of cocoa yesterday and only brought up 16 ozs. 



He is having peptonised milk, which he also manages to keep 
down. Is having nntrient enemata of milk and beef-tea. Pulse 
128. Inspirations 28. Temperature 97° this morning. During the 
last few days he had developed a papular rash. The papules are 
red, raised, and some pustular, distributed widely all over the 
baok, also to a less extent on both arms and chest. None on 
abdomen. They vary in size from a pin’s head to a small bead 
(iod. rash). Last night had ni ii. croton oil. 

May 21.—Slept better last night, complains of a bitter feeling 
in his stomach which causes him to retch a good deal. Is having 
4 ozs. brandy. Pulse 132. inspirations 30. Urine dark ammoni- 
cal. Specific gravity, 1,020. Deposit of urates. 

Says that the pain in his head is much less severe this morning. 
Slept well last night , and for the first time since admission. Did 
not require the morphia hypodermic injection. Arms not so tender 
this morning. 

May 22.—Had to have an injection of morphia before he could 
get any sleep last night. The pain in the head is fast disappear¬ 
ing. Still vomits a good deal. Pulse 108. Respirations 24. 

May 23.—Had an injection of morphia last night before he 
could sleep. Complains of pain across the abdomen. Vomits up 
everything he takes. Pulse 120. Respirations 32. 

May 25.—Twelve grains of potassium iodide added to each 
nutrient enema, which is given every four hours. 

May 26.—Had to have an injection of morphia again last 
night before he could sleep. Pain still present across the abdo¬ 
men. Condition seems much improved. Still a little pain in the 
head. Pulse 90. Respirations 18. He is having ung. hydrarg. 
rubbed into each axilla, alternately, night and morning. Has not 
vomited at all to-day. So far he can keep down beef-tea, bread 
and butter and weak tea. 

May 27.—Nutrient enemata, each containing 25 grains of 
potassium iodide, ordered to be given every six hours. Each 
alternate enema to contain in addition tr. opii. uixx. Patient’s 
condition is improved. 

May 28.—Passed a good night, now has slight pains in the 
head and very slight pains in the limbs. On the whole he seems 
much easier than before. Eight p.m.—During to-day he has 
vomited 10 ozs. in all. He has taken plenty of milk and beef-tea 
by the mouth, a considerable quantity of which he has retained. 
Bowels opened once this evening without enema. 

May 29.—The tenderness has disappeared from the head 
except just at the back. The hyperesthesia has nearly disap¬ 
peared from the legs and arms. 


May 30.—Feels much better this morning. Still feels pain in 
the abdomen and limbs. Measurement of limbs :— 

Left leg 9 inches above internal maleolus ... 10J inches. 

Bight leg ,, ,, „ ... 9| inches. 

Left forearm 3 inches below internal condyle ... 10J inches. 

Bight forearm „ „ ... 9 inches. 

Left arm 4 inches above internal condyle ... 9£ inches. 

Bight arm „ „ „ ... inches. 

Cannot sleep at night without his injection of morphia. 
Pulse 96. Bespirations 24. Urine dark, neutral, specific gravity 
1,027, no albumen, no sugar. Did not vomit at all yesterday, nor 
during the night, nor this morning. Slept well last night after tbe 
morphia injection, which he found it necessary to have on 
account of the abdominal pain. 

June 1.—Slept last night without morphia injection. The 
scalp is less tender at the back than it was. Complains of pain 
in the left leg and back this morning. The abdominal pain is not 
so bad as it was. He has not vomited at all since Thursday. 
Pulse 90. Bespirations 18. Urine : medium, ammoniacal, specific 
gravity 1,011. Deposit of phosphates. The hyperesthesia has dis¬ 
appeared from the right arm and leg, but has not yet disappeared 
from the right limbs. Milk is now given by the mouth unpepton- 
ised, with 1 oz. of liq. calcis seech, to each feed. Nutrient 
enemata with potassium iodide reduced from four to three times 
daily, and the tr. opii. is now only to be given with the last enema 
at night. 

June 3.—Slept well without the morphia injection. The 
vomiting has quite passed off now. Only very slight tenderness 
on pressure of the limbs. The scalp is hyperesthetio at the back 
and sides, not at the front. Pain in the abdomen still continues, 
and there is still slight pain in the legs. He is having fish. 
Urine: cloudy, 1.010, acid. No deposit, no albumen. Pulse 
108. Bespirations 42. 

Measurement of legs and arms : The only difference is in the 
left arm, which is 10 inches round 4 inches above internal condyle, 
an increase of -f- of an inch. 

June 4.—Slept very well last night without the injection. 
Tenderness of the scalp and limbs remains the same. Pulse 114. 
Urine slightly alkaline. Specific gravity 1,011. No albumen, no 
sugar. Complains of his eyesight not being so good this morning. 

June 6.—Slept badly last night. Complained of pain in the 
stomach. Is having his arms and legs massaged now. Tender¬ 
ness of the limbs and hyperesthesia of tbe scalp are diminishing. 



Urine, acid. Specific gravity 1,023. No albumen, no sugar. 
Pulse 90. He is having by the mouth, with milk, potassium 
iodide 25 grains. 

June 8.—Complains of shooting pains in the back of his head 
this morning, also pain in the abdomen. He had antipyrine, 10 
grains, yesterday morning. Thinks the massage is doing him 
good. Pulse 90. Respirations 30. 

June 9.—Patient’s head is a little easier this morning, and 
the pain in the abdomen is diminished. Pulse 90. 

Measurement of legs, 9 inches above internal condyle. Right 
9f, increase $ inch. Left 10J, increase of £ of an inch. 

Left forearm 10£ inches, increase of £ inch. 

Right forearm 9£ „ ,, i »» 

Right arm 8} „ .. i 

Left arm 10£ „ „ | „ 

June 10.—Had a restless night. Complains of pain in the 
abdomen still. Had fish yesterday. 

June 12.—Patient had a very bad night. Complains of shoot¬ 
ing pains all over his head this morning. 

June 13.—Slept very little last night. Pains in the head are 
worse this morning, and he complains of pain across the abdomen. 

June 15.—Patient got up yesterday, but vomited twice, so 
went back to bed again. Pain in the abdomen is a little easier 
this morning. Head remains in the same condition. 

June 16.—Seems more cheerful to-day. Had a restless night. 
Tenderness of the scalp unaltered. Pain in abdomen much easier. 
Having chicken for dinner to-day. The massage treatment which 
patient has been undergoing seems to have improved the limbs. 
The movement of opposition of the thumb on the right side, 
which before was absent, is now present. Urine, acid. Specific 
gravity 1,014. No deposit. 

June 17.—Had a sleepless night. Complains of feeling sick 
this morning. Managed to keep some chicken down yesterday. 

June 18.—Slept fairly well last night. Complains of the heat 
a good deal. Has developed a papular eruption at the upper and 
inner part of the thighs. 

June 19.—Not so well to-day. Has been sick three times this 
morning. Vomiting commenced at 9 o’clock. Urine: specific 
gravity 1,014, bright, acid. No albumen, no sugar, no deposit. 

June 20.—Not been sick yet this morning. Sick three times 
last night. Complains of his arms commencing to get tender 

June 22.—Does not feel at all well to-day. Complains of 


pain in right arm, leg, and head. The eruption at the upper part 
of the thigh presents a dried-up vesicle. 

June 24.—Seems slightly cyanosed. Is not feeling very well 
this morning. Has vomited once. Urine: specific gravity 1,012, 
acid, bright, mucous cloud. No deposit. Papular eruption covers 
his back and the upper part of his thighs. He brings up a rusty- 
looking muco-purulent expectoration. 

June 25.—Complains of the pain in his stomach being worse, 
otherwise he looks and feels a good deal better this morning than 

June 26.—Not quite so well to-day. Vomited before breakfast, 
but has not done so since. Pain in the abdomen rather worse 
this morning. 

June 27.—Looks a little better. Has not vomited since 
yesterday before breakfast. 

July 1.—Scalp rather tender this morning. Soreness of gums. 
Potassium iodide has been reduced to 15 grs. 

July 7.—Not quite so well this morning. Tongue furred. 
Sat up for one hour last night, but was sick afterwards. An 
inflamed spot has developed over the head of the fibula on the 
right side. The surrounding tissues are rather tender. 

July 9.—Much better this morning. Still complains of sore¬ 
ness of the scalp. Got up for one and a-half hours yesterday. 
Did not feel sick afterwards. 

July 13.—Was up all day yesterday. Did not feel sick at all. 

July 14.—Up all yesterday afternoon. Pelt sick this morning. 

At the end of July he was discharged, relieved of all the 
acute symptoms of meningitis, but in a partially paralytic 

Case 20.— 

T. R.—Syphilis eighteen years ago. Secondary symptoms. 
Treated with mercury and iodide. Twelve years after infection 
suffered with left hemiplegia. Dimness of vision in the right eye 
for which he attended Moorfields. Now there is old left hemi¬ 
plegia and optic atrophy in the right eye. 

Case 21.— 

W. F. f aged 31, occupation, clerk. Syphilis fourteen years 
ago. Sent from the Ophthalmic Hospital. He has paresis of 
right side of face with clonic spasm of the orbicularis palpe¬ 
brarum. Tongue protruded to left. No affection of speech. 



Large absolute scotoma for red and green in right eye. Smaller 
for left eye. Alcohol in great excess, also tobacco. Pupils equal, 
react to light and to accommodation. Ophthalmoscope. — 
Vessels full, with broad reflexes. Some striation about the 
optic disc, making the margins rather indistinct. 

Case 22.— Probable anomalous case of tabes dorsalis, commencing 
with symptoms of basic syphilitic meningitis. 

E. C., male, aged 34, Polish Jew, tailor. Had syphilis twelve 
years ago and was treated for a fortnight. Came to Charing 
Cross Hospital in March, 1898, suffering with ptosis of the right 
eye, double vision, frontal headache, and lightning pains in the 
legs. The double vision and squint was due to paralysis of the 
right internal rectus. The pupils were equal, medium-sized, and 
reacted to accommodation but not to light. The knee-jerks are 
brisk on both sides and there is no ataxy. He was treated with 
mercury and iodide for a month, but I did not see him again till 
October, 1898, when the following note was made :— 

Ptosis and external strabismus of right eye. Double vision. 
Argyll-Bobertson pupils. Lightning pains in legs. Bight knee- 
jerk present but diminished. Left knee-jerk brisk. No ataxy. 

March 4, 1899.—Patient came with complete paralysis of the 
right third nerve. Ptosis, external strabismus and immobility of 
the eyeball. Both pupils equal, medium size, inactive to light 
and accommodation. No ataxy, can stand on one foot. No 
Bomberg’s symptoms. Has not had any pains in the legs lately. 
No girdle sensation. Has had some difficulty in passing water 
and recently he has had severe rectal tenesmus coming in 
paroxysms and causing him great suffering, probably rectal 
crises. The knee-jerks brisk on both sides. No tremor of 
tongue or face. No speech affection. Mental condition normal. 

Case 23.— Probable gummatous meningitis, eight years after infec¬ 
tion, producing paralysis of spinal accessory and hypoglossal 
nerves of the right side, causing unilateral paralysis of soft 
palate and vocal cord, with paralysis and atrophy of the right 
half of the tongue. 

W. W., male, aged 36; 'bus driver. Discharged from the 
army in 1892; oame to Charing Cross Hospital, March 22, 1899. 
Sent from the Throat Hospital, Golden Square, by Dr. Bond, who 
has kindly permitted me to use the notes. 


History .—Contracted syphilis in 1890, for which he was 
treated for three or four months. He gives a history of intemper¬ 
ance, and has an appearance of such. Last September he had a 
swelling in the throat and inability to swallow. He suffered with 
sickness, severe headache, deafness in the right ear, and swelling 
in the left side of the neck. He attended Dr. Bond at the Throat 
Hospital, and he has greatly improved under iodide of potassium. 

Present condition .—The patient has a brassy clanging cough. 
He can only speak in a hoarse whisper, and his gait is feeble. 
Signs of syphilis on the body—there are enlarged cervical glands 
and a great number of small scars all over the front of the chest 
and back. The pupils are unequal, the left 5$ mm., the right 
4£ mm. Respond sluggishly to light, react well to accommoda¬ 
tion. They respond fairly well, however, to a strong light. 
Knee-jerks exaggerated. No wrist tap contraction, nor jaw 
clonus. Superficial reflexes normal, no loss of sensation. The 
tongue, when protruded, deviates markedly to the right side. 
There is marked atrophy of the right half of the tongue. The 
patient says that at one time he could not move the tongue to 
touch the right cheek. There is no loss of tactile sensation in 
the tongue, nor is there any loss of taste. 

Examination of the throat .—The right arch of the fauces is 
lower than the left, the uvula deviates to the left, and on telling 
him to say “ Ah 1 ” there is obvious paresis on the right side of 
the soft palate which scarcely moves. There is no paralysis of 
the sterno-mastoid or trapezius. Examination with laryngoscope 
showed complete paralysis of the right vocal cord. There is 
defective movement also of the left, but I am informed by Dr. 
Bond that this has considerably improved. His sight is good 
and nothing was discovered in the fundus. Hearing good; he 
can hear a watch at a distance of a foot from either ear. Three 
months ago he complained of noises continually in his ears, but 
he says that the medicine he has had has completely made a new 
man of him. 

Case 24 .—Probable syphilitic endarteritis ami thrombosis, causing 
temporary aphasia and hemiplegia. Restoration by collateral 

E. N., aged 39, female, needlewoman ; admitted into Charing 
Cross Hospital on March 8, 1899, for aphasia aud slight right¬ 
sided hemiplegia. 

Past personal history, which was only got after the patient 
had regained her power of speech. She says that she had 



“ brain fever ’’ when about 12 years of age. She does not 
remember much about the illness, but thinks that she was ill for 
about .six months. No other illnesses. She was first married 
when she was 22 years of age. She had no children and no 
miscarriages. Her husband died, and she married again seven 
years ago. She had one child (full term) about a year after 
marriage. It died at the age of three months of bronchitis. It 
was a healthy-looking baby and never had snuffles or rashes. 
She has had no miscarriages. Patient attended the out-patient 
department of this hospital about eighteen months ago for a 
“ sore place ” situated at the lower part of the back. Patient 
says she was given medicine, but it was about nine months before 
it quite healed up. She had no other ulcers about her body and 
there is no history of sore throat or rash. Dr. Galloway tells me 
that he at first thought it was a non-specific sore, but it only 
healed up when treated with iodide, and he came to the con¬ 
clusion that it was of syphilitic origin. 

Present illness .—Up to the afternoon of Wednesday, March 
8, patient was feeling perfectly well. She had no headache or 
premonitary symptoms whatever. She had been at her usual 
work (sewing) and got up from the table to go downstairs when 
she suddenly fell, and at the same time she lost her power of 
speech. She noticed nothing unusual about her arms and legs. 
A doctor was sent for immediately, but, as he was out, patient 
was put in a cab and brought round to the hospital. The man 
who brought her to the hospital said that after falling she was 
unable to speak, but he does not think that she was at any time 
unconscious. He did not notice anything wrong with her face or 

Patient was seen by a house physician in the casualty room 
about an hour after the fit. She was seated in a chair. She did 
not reply to any questions but made an inarticulate noise when 
spoken to. The right corner of the mouth was noticed to be 
lower than the left, but it was found that several teeth were 
absent on the left side (lower jaw). Patient would not grip a 
hand when told to do so and it was not easy to discover whether 
there was any loss of power of the right arm. Both knee-jerks 
were present but not exaggerated. Her gait was not tried. She 
did not seem to understand the questions that were put to her. 
Tongue was protruded straight. She was taken up to the ward. 
At first she refused to swallow some milk, but after a great deal 
of difficulty she was made to swallow a mouthful and after that 
she had no difficulty. Her heart and lungs were found to be 
normal, as was also her urine. There was a shiny, somewhat 


pigmented scar situated over the centre of sacrum which had 
irregular edges and presented the appearance of being an old 
syphilitic ulcer. The skin on the legs was normal, and there 
were no glands to be felt. The following day, after about twenty- 
four hours, patient managed to say “ yes ” and “ no,” and during 
the second she regained the power of speaking a few words, but 
could not string them together in any form. She hesitated 
considerably, as if she were trying to think of a word or else 
endeavouring to form it. At first she did not appear to recognise 
objects that were shown to her, but she gradually regained this 
power, and about thirty-six hours afler admission she mentioned 
the names of some common articles that were shown to her, but 
could not recognise others even when the names were correctly 
mentioned to her. She appeared unable to write when asked, 
the only result being her age in figures, and these were so badly 
formed that it wa3 thought to be thirty-seven and not thirty-nine. 
When asked she shook her head at the first number, and affirmed 
when the second was suggested ; this latter turns out to be the 
correct age. The right angle of the mouth is slightly lower than 
the left. On showing her teeth nothing definite could be made 
out, hut on screwing up both eyes there was a loss of muscular 
action on the right side. The tongue is now protruded slightly 
towards the right. Her arms are fairly well developed, but the 
grip is not so well marked on the right side as on the left. The 
finer movements of the fingers of the right hand are impaired, as 
the patient picks up small articles much more readily with the 
left hand. Tendon reflex is markedly increased on the right side. 
Her legs were very well developed. There was some loss of 
power in the right leg which was best shown when the hip was 
flexed against resistance. The knee-jerks were greatly exaggerated, 
rather more so on the right side. Ankle clonus was well 
marked, regular and persistent on the right side, an attempt at 
clonus on the left side but not so marked. Patient was put on 
potassium iodide on March 8, 10 grs. being given. This was 
increased to 20 grs. on the 11th, and her improvement was very 
marked. On March 13 this dose was increased to 30 grs. Her 
improvement is very marked, there being a noticeable difference 
in her speech. To-day (13th), she can speak well, although at 
times she has to hesitate before she can form a word. Her 
memory, which was impaired, has returned, and she says that 
her present hesitation is due to her not being able to form the 
word, although she knows what she wants to say all the time. 

March 17. Patient got up to-day and was able to walk 
without any assistance. The signs of hemiplegia have dis- 



appeared with the exception of the drooping of the right angle 
of the mouth. The clonus has quite disappeared these last two 
days. Her knee-jerks are not now so exaggerated, and neither 
is the tendon reflex of the right arm. She takes her food well. 
Her temperature has been always normal since admission. 

When patient regained the power of speech it was found that 
she was naturally left-handed in some of her movements. She 
held her needle in her right hand but always cut with scissors 
with her left. The left-handedness was very limited, however. 


Case 25.— Syphilitic brain disease. Dementia and paresis following 
one year after infection. History of alcoholism. The paraly¬ 
sis followed a fit. 

H. S., aged 37, married, a horsedealer; admitted September 
17, 1898. Admitted to Hanwell for dementia and paralysis. 

Personal history. —Was always well and steady, a good 
husband and father up to two years ago, when his wife, after a 
quarrel, left him. Since then he has drunk heavily, and con¬ 
tracted syphilis twelve months before admission; he was under 
treatment at the Lock Hospital, but informant (his father) does 
not know for how long. Nine weeks before admission he had a 
“fit” followed by “delirium.” As far as his father knows, he 
was perfectly strong and well up to that time, but since the fit 
he has gradually become more and more “ paralysed.” 

Condition on admission. —Mental—He is demented, less 
vacant and confused; he has a dreamy expression and takes no 
interest in his surroundings, memory for both recent and remote 
events greatly impaired. Bodily—He is thin and wasted, is 
unable to walk and lies in a drowsy, semi-conscious state, from 
which, however, he is easily roused. Evidences of a very severe 
attack of syphilis, a large number of scars on legs, arms, trunk and 
face; they are very typical; depressed, pigmented, “ punched 
out ” some as large as five-shilling pieces. An active syphilide, 
eczematous rash on left arm and over left eyebrow. Tongue— 
chronic glossitis; it is enlarged, bared of epithelium and fissured. 
Gums inflamed; says his mouth and throat have been “ sore.” 
Lungs, healthy. Heart—second aortic sound accentuated at 
base, otherwise normal. 

Nervous system.— Motor—Although he is quite unable to make 
any effort to stand, there appears to be no paralysis of any 
muscles or groups. Flexion and extension of both knees and 
ankles powerful. Slight superciliary tremors and slight labial 
tremors. No loss of labial folds. Eye movements normal. 


Muscles of calves greatly wasted, thigh muscles also wasted, left 
more so than right. Tongue protruded in mid-line, fine tremors. 
Sensation—Tactile; nothing abnormal, appreciates heat and cold. 
No muscular tenderness or pain. Sight—pupils equal, small* 
react to accommodation; slightly also to light. No hemianopsia. 
Reflexes—Superficial: plantar well marked. Deep: knee-jerks 
quite lost; no ankle clonus; no elbow or wrist-jerk; jaw-jerk 
present. He passes his urine and stools in the bed. Speech— 
normal, no hesitation, drawling or stuttering, consonants not 
sharply pronounced, speaks like a man half asleep. 

Progress of patient. —Was placed upon iodid. potassii, which 
was gradually increased to 60 grs. per diem on November 1. 
Has remained on this until this week, when it has been increased 
to 75 grs. per diem. On my return to the Asylum in the middle 
of February I found that the syphilide rash on left arm and fore¬ 
head had entirely cleared up. His bodily condition was greatly 
improved, face and trunk fattened out and healthy-looking. He 
still, however, sleeps during almost the whole of the day; is 
easily roused to take his meals, but relapses again immediately 
after. He still passes his urine and stools in the bed, while in 
this drowsy state, but asks for assistance if he happens to wake 
up. Is always quiet; rarely speaks and has had no fits while 
here. During the last two days (March 10), superficial sores 
have again appeared on both ears and left side of chest. He is 
still quite unable to stand; this appears to be due more to inco¬ 
ordination than to paresis of muscles. Notes by Dr. Sparkes. 
Ophthalmoscopic examination revealed no optic neuritis. — 
F. W. M. 

Case 26.— Case illustrating brain syphilis coming on in a young 
man within three years of infection. No primary sore, only 
urethral discharge, but enlarged glands, rash, and sore throat. 
The exact period of infection could not be determined. Im¬ 
proved markedly under anti-syphilitic treatment. 

Admitted to Charing Cross Hospital for weakness of left arm 
and leg. 

Past personal. —Patient has always been pretty healthy ; had 
gonorrhoea three years ago, the discharge lasted altogether about 
three months. A few weeks after the gonorhoea the left testicle 
became swollen, and very painful and tender; about twelve 
months later the left knee suddenly became inflamed. No injury 
that patient can remember; he went to hospital, and his knee 
was strapped and put on a back splint for three weeks. It is 



possible that he may have been infected with syphilis since, for 
he has had frequent connection, but he has never noticed a sore. 
Patient says that he did not have a sore at the time of the 
gonorrhoea, and has never noticed one since. For the past six 
months patient has been suffering from severe headaches; the 
headaches more frequently occur on the left side of the head and 
left eye; they often kept him awake at night to such an extent 
that on several occasions he has had to sleep during the daytime 
when the headache has been better. Patient had headache 
during the week previous to his present attack, but not worse 
than usual. No premonitory symptoms in the arm or leg occurred, 
but he experienced some difficulty in buttoning his clothing; 
this condition got no better, so patient came up to hospital, 
and was admitted on Saturday, April 1. 

Condition on admission. —Face : rather pale ; no signs of 
paralysis; tongue protruded in mid-line; muscles on both sides 
move well and equally; no ocular paralysis; no tenderness over 
right Bolandic area. Arms—left forearm shorter and thicker 
than right, evidently due to an old fracture that patient sustained 
when a boy ; he says that up to present illness his left arm has 
been as strong as his right. There is marked weakness of the 
grip on the left side; flexion and extension at elbow not much 
affected. Tendon reflexes markedly exaggerated. Tactile sensa¬ 
tion appears normal. Legs—no wasting of muscles ; position of 
limbs normal; loss of power in left leg as compared with opposite 
limb; knee-jerk exaggerated; loss of superficial reflex; slight 
ankle clonus (sustained and regular). 

General examination. —Chest—there is a fading rash about 
chest, and abdomen, and shoulders, papular, dull red in colour, 
becoming brown. Heart and lungs normal. Urine normal. 
Patient complains of sore throat, which be first noticed the day 
after admission. On examination, the back of tbe pharynx is 
red, tonsils not enlarged, no signs of ulceration. (Patient says 
that the rash first appeared 3 to 4 months ago, and has persisted 
ever since.) Examination of genitals—Lips of meatus stuck 
together with slight mucous discharge (this the patient had not 
noticed), no chancre about penis to be seen, two small scars on 
glans penis, no intra-urethral chancre can be felt. Left epi¬ 
didymis can be felt; not tender. Testicles otherwise normal. En¬ 
larged, discrete, and hard glands to be felt in both groins. Some 
enlarged glands to be felt in neck on both sides (upper cervical). 
Temperature normal; weight 8st. 61b. B. regular. April 10.— 
Patient is now on pot. iod. gr. xv. t.d.s. He is having mercury 
ointment rubbed into abdomen daily. Garg. pot. chlor. for throat 


and month; iii. diet. Uses tooth brush after every meal. Bash 
has faded a good deal since admission. Throat less sore, still 
red, no ulceration. 

Case 27.— Case of tabes dorsalis commencing with, symptoms which 

might be, and actually were, mistaken for brain syphilis. 

T. B., male, aged 41, tailor, who came from the B. W. 
Ophthalmic Hospital, where he had been under treatment for 
double optic atrophy for the last six months. He complains of a 
sense of constriction around the forehead, also sharp shooting 
pains in both thighs. He has no pains about the trunk. Patient 
contracted syphilis about ten years ago, and was under treatment 
for eight weeks. He says that the first thing he noticed was 
double vision in March, 1897, eleven months ago. He did not 
have any squint. About fourteen weeks ago he had dimness of 
vision, and six weeks ago he lost his sight completely. He had 
no headache, no sickness, no paralysis, but frequent micturition 
and shooting pains in thighs. For six weeks he has had a pain 
over the frontal region as if a tight hat were pressing on his 
forehead. His eyes are prominent and there is a slight degree of 
exophthalmos. There is some loss of expression in the face. 
The knee-jerk is very slightly diminished on left, but marked on 
right side. There is no girdle sensation. There is grey atrophy 
of discs. The vessels are normal in size and the discs very 
distinct and of a greyish-white colour. A fortnight later the 
knee-jerks entirely absent and the pains quite gone, but every 
now and then he has great difficulty in breathing. The fre¬ 
quency of micturition has, in a measure, passed off. There is 
a little numbness in the toes. He can stand still with heels 
together. Gait not ataxic. He has no loss of sense of position. 
He can touch tip of nose with forefinger accurately. 

March 9, 1898.—He feels better and has no pains now. The 
knee-jerks are now quite absent. His pupils are rather large 
but equal, they react to accommodation but not to light. There 
is no ataxy either when walking or standing. 

May 4, 1898.—He complains of spasm in the throat and 
sudden difficulty of breathing, which lasts a few minutes; fre¬ 
quently this spasm is excited by cold or hot fluids. Has no 
more lightning pains in the legs. Says he has pain in the larynx 
when the spasm is on but not in the skin over it. Laryngeal 
crises. He has no difficulty in passing water. 

October 12, 1898.—Patient is still in the pre-ataxic stage, but 
suffers no pains now. There is nothing fresh to note and the 



disease is apparently stationary. He has found that the anti¬ 
pyrin administered in ten-grain doses has given relief, both for the 
pain in the legs and the laryngeal spasms. 

Case 28.— To illustrate brain syphilis followed by dementia and 
paralysis, treated in a number of hospitals, but gradually pro¬ 
gressing, and finally the patient becomes an infirmary patient, 
and lastly an asylum patient. It also illustrates remissions of 
the symptoms and a class of case pretty common in asylums 
and workhouse infirmaries, and which for a long time becomes 
a source of expense to the ratepayer. 

J. P., aged 40, single; occupation, sanitary engineer's 

Admitted into Hanwell Asylum on April 28, 1898. 

Patient has been paralysed for eight years. He drank heavily. 
He declines to say how long ago it was he had syphilis. Scar on 
penis. Breaking down gummata over right clavicular region. 
Diplopia. Pupils dilated. Slight ptosis of right eye. Slight 
giddiness eight years ago was the first indication. Then pain in 
oalves of legs, then weakness. He was an out-patient at Middle¬ 
sex Hospital under Dr. Fowler. He took medicine and got better. 
He was not long attended. Eight or nine months later he had 
another attack of general weakness, but chiefly in arm with 
staggering gait and double vision. He was under Dr. Sharkey, 
8t. Thomas’, for a considerable time, then he was able to walk 
about and go to work again. About twelve months later he had 
another attack with general weakness. No vomiting or headache. 
Diplopia persisted all through, after first attack. He then became 
a patient at Queen Square, under Dr. Buzzard (H. P., Dr. 
Taylor). He got very much better, but was unable to go to work. 
He stayed at home for twelve months. Then he went back 
to Queen Square. He has been in St. George's, Middlesex, 
and also in Guy’s, under Dr. Goodhart. 

Present condition. —Pupils unequal, left larger than right. 
Do not react to light or to accommodation. Sight imperfect. 
Slight ptosis of left eye, but absolutely no movement of left eyeball 
in the four directions. Tongue deviates to left. Facial paresis on 
left side. Can close eyes, hut no marked paralysis. No tremors. 
He has control over his sphincters. No dysarthria noticeable, 
not even with lip explosive sounds. There is wasting of both 
arms, but the right hand is especially affected. All the small 
muscles are affected by an atrophy. Knee jerks, he says, have 
been absent for years. He had numbness of the hands and had 


pains in the back of the head and neck, with stiffness. Great 
weakness in hands. He cannot sit up. There is wasting of the 
back muscles, and the leg muscles are greatly wasted. The 
plantar reflexes are present more on the left side than the right. 
Knee-jerks absent. He says his sensation is perfect except the 
hands. He says his taste is slightly impaired. Did not recognise 
milk or bitter fluid. Bight abdominal reflex present, left lost. 
Sense of position of hands lost. Has a delusion that the authori¬ 
ties of Chelsea Infirmary are pulling at his bowels. 

August 7.—There is drooping of left eyelid and weakness of 
right side more marked than left. His speech is unaffected and 
his sight is good. He recognised me quite well, but was surly 
aud wished to know what right I had to ask questions. 

April, 1899. Still in the same condition. 

Case 29.— E. S., epileptic, aged 25, spinster, was transferred to 
Claybury Asylum, from the Workhouse, where she had been an 
inmate for five or six years. She is afflicted with left hemi¬ 
plegia with contractures, probably due to congenital syphilis. 

History. —The paralysis came on when she was about 12 
months old, with convulsions attributed to teething. During 
childhood and girlhood she had frequent convulsions, sometimes 
many in a day, these being followed by more or less protracted 
unconsciousness. Of the duration, progress and nature of the 
fits she can give no account. They appear to have become less 
frequent of late years, and according to the attendant have not 
occurred since she has been in the asylum. Beyond measles she 
remembers no other illness. She has never been able to earn 
her living. 

Family history. —Both parents dead. Her mother was a 
confirmed drunkard, and the father also is said “ to have taken 
his glass,” but was not an habitual drunkard. Patient is one of 
six children, of whom an older brother and sister are still living, 
but she is unable to give any further account of them or of those 
dead. In view of the condition of patient’s eyes, the family taint 
of syphilis as well as that of alcoholism, may be present in her 

Present condition. —Patient is a fairly well nourished woman, 
of medium height, with a gentle, somewhat weak-minded expres¬ 
sion. The complexion is muddy, the face asymmetrical, the 
head inclined to the left, sometimes slightly extended, more often 
flexed. A left external strabismus, slight dribbling from the left 
corner of the mouth. The left arm is atrophied and contracted, 
and the left leg also to a less degree. 



Mental condition .—Patient ia able to give a fairly intelligent 
account of herself, and answers connectedly questions put to her. 
Her memory appears fair and she is able to give the ages at 
which she lost her parents, and to state where she has lived. 
She is able to spell her name, hut her education does not appear 
to go much further. Concentration is very defective. She is 
said to sleep well and to have no delusions. In character she 
appears gentle, quite emotional, easily amused, but not getting 
boisterous. She is reported as docile and industrious generally, 
but has violent fits of anger when teased. 

Neuro-muscular system .—The left side of the face is altogether 
smaller than the right, the lower muscles of that side being in a 
state of overaction, due to spasm which has drawn the nose and 
mouth to the left. This becomes more noticeable when she smiles, 
and there is a spasmodic twitching of the lips on the left. The 
folds on the forehead are equal. The eyes shut equally, and the 
movement of the eyes is good. There is some contraction of the 
muscles of the neck, but the head can be held straight by an 
effort of will. The right arm is normal, but the left is paralysed 
from the elbow downwards. It is held with the elbow flexed at 
a right angle, the forearm pronated, the wrist flexed and the 
fingers folded into the palm of the hand, the thumb being tucked 
in and the little finger only extended at the phalangeal joints. 
The movements at the shoulder are perfect, but neither the elbow 
nor wrist permit of active or passive extension. The inter- 
phalangeal joints of the fingers can be passively straightened. 
The right leg is normal and the left is slightly shorter and smaller 
than the right. The movements at the hip and knee are perfect, 
but the foot is in a position of very slight equino talipes with the 
toes hyper-extended, and permits very slight extension at the ankle 
joint, while very little flexion, either active or passive, is possible. 
In walking, there is some dragging of the left toes along the ground, 
the left foot is lifted rather higher than the right, and there is 
some inco-ordination of movement. The skin of the affected 
parts is everywhere normal, the nails are good, but there is 
impaired growth of the bones and muscles. The ulnar and 
patellar reflexes on the left side are exaggerated. Plantar reflex 
active on both sides, more so on left. 

The tactile sensation is not impaired. Pain and temperature 
not tested. Taste not tested. Hearing good. Vision impaired, 
owing to the following structural changes :—There is left external 
strabismus. The palpebral fissures are equal. The movements 
of both globes are good. The pupils are large and active, on the 
left cornea there is leucoma, on the right there is a central 


nebula, fairly dense, visible in a good light. With the left eye 
she counts fingers at several feet, with the right she can dis¬ 
tinguish letters. Vision not further tested. 

Ophthalmoscopic examination. —Patient fixes badly, and the 
illumination of the left fundus is rendered difficult by the condi¬ 
tion of the cornea, but a fair view of both fundi was obtained 
by the direct and indirect methods. In both a condition of 
choroido-retinitis is present, apparently extensive, but localising 
is difficult owing to constant movements of globes. The 0. D.’s 
are misty, both small vessels; there are large masses of dark 
pigment, sometimes in round blobs, sometimes in spider-shaped 
masses. In the left eye round, yellow spots were detected, but 
not localised. 

Her tongue is fissured; her teeth bad, palate normal, 
appetite good, bowels said to be regular. No thorough examina¬ 
tion made. Breathing and heart’s action regular. Arteries 

Diagnosis. —Patient is probably suffering from the results of 
infantile hemiplegia due to some cortical lesion either vascular 
or inflammatory in origin. There is probably now a condition 
of sclerosis of the right hemisphere affecting chiefly the motor 
convolutions, but possibly the hemisphere as a whole. The 
paralysis has been followed by spasm of the affected muscles 
and the disturbance of innervation by lessened growth of the 
bones and muscles involved. The fits, epileptiform in character, 
are probably due to irritation caused by the sclerosis of the 
brain. They are probably unilateral to begin with. The mental 
condition is owing to the defective development of the brain as 
a whole and is one of weakness of mind not amounting to 

Case 30.— Brain syphilis and meningitis, probably with gummatous 
tumours eighteen months after infection. Great improvement 
under treatment. 

F. G., 9828, aged 24, formerly able-bodied seaman, Boyal 
Navy. Admitted to Hanwell, September 30, 1898. Contracted 
syphilis eighteen months ago in China; sore throat, and hair 
came out followed by rash. Treated for six weeks. (? reliable.) 
He has now a number of large pigmented patches on both legs, 
and enlarged iuguinal and cervical glands. The illness com¬ 
menced with severe headaohe, which kept him awake at night; 
pains in the back and stiffness of the neck. A little later double 
vision. He is now suffering with paresis of both arms and legs. 



the weakness being more marked on the right side, so that the 
tongue deviates slightly to the left, and there is a little more 
paresis on the right side than the left, which becomes obvious 
when he shows his teeth or smiles. There is no loss of sensa¬ 
tion, the superficial reflexes are present, deep reflexes exaggerated, 
ankle clonus on both sides. He has completely lost the sight of 
the left eye. Pupils : right measures 7 mm., left 5£ mm. Neither 
react to light, but to convergence. The paralysis came on sud¬ 
denly after a fainting fit. His utterance is thick and articula¬ 
tion somewhat indistinct. He tries to express himself, but his 
memory is very bad as he makes the most contradictory state¬ 
ments. He is in a drowsy, stupid condition, but will answer 
questions and can talk about his past life, and remembers the 
name of the ship and the stations he was at. His appetite is 
fairly good and he has nothing wrong with his smell, taste, or 
hearing. Beyond the headache he has no pain. He now com¬ 
plains of no stiffness in the neck. 

February 15.—Patient is a little more active in mind and 
body. There is a little more expression in the face, but there 
is still some right facial paresis. Weak grasp in both hands, 
especially the right. All the muscles are wasted, especially the 
arms. Wrist tap contraction obtained on the right side easily. 
Less marked on the left. Knee-jerks not markedly exaggerated 
now. Pupils are still unequal, right larger than left. Bight 
reacts to light and to accommodation. 

Ophthalmoscopic examination.— Fundus of the left eye has a 
greyish-white appearance, edges sharp, vessels normal in size, 
not curved. Improvement marked since I last saw him due to 
the treatment with 30-grain doses of iodide of potassium three 
times a day. 

April 4th.—Still improving mentally and’ bodily. He has no 
control over bladder during the night. Recommended that he 
should be awakened twice during the night to pass water. 

Diagnosis. —Syphilitic, basic and spinal meningitis, probably 
gummata and arteritis as well. 

Case 31.— Brain syphilis commencing as meningitis with ptosis 
eight months after infection although under mercury the whole 
time. A few months later arteritis, thrombotic occlusion, fit 
followed by hemiplegia and dementia. 

E. J., aged 36, widower ; admitted into Hanwell. Contracted 
syphilis eighteen months ago. Followed by sore throat and rash. 
.Treated at the Lock Hospital. He has never suffered with head- 


ache. Twelve months ago noticed drooping of the eyelid, althoagh 
he bad been treated with mercury pills for quite six months. Six 
months ago had a fit, followed by paralysis of the right side, 
affection of speech and dementia. 

February 15.—Much better mentally. Pupils equal and 
react to light and to accommodation. Still slight ptosis on left 
side, facial paresis on right side. All the deep reflexes ex¬ 
aggerated. Jaw-jerk ; wrist-tap ; knee-jerk ; ankle clonus. 
Tongue deviates to the right; still marked thickness of utter¬ 
ance. Suffering with ozsena from necrosis of the upper jaw. 
Improvement in symptoms due to treatment with mercury and 

April.—He is still hemiparetic, but he is improving mentally. 

Case 32.— Sensory facial aura and taste in mouth. Transitory 
aphasia followed by a fit. Syphilis twelve years before. Im¬ 
proved greatly under treatment. 

W. F., aged 38. Came as an out-patient to Charing Cross 
Hospital, January, 1899. The following notes were taken. 
Occupation, packer. Has served in the army twelve years. He 
has been in South Africa and in India. Contracted syphilis 
twelve years ago, for which he was treated for three weeks. He 
had a bubo ; most probably it was a mixed infection, for secondary 
symptoms developed in the form of sore throat, rash, and loss of 
hair. He is married, and has three healthy living children. He 
married three years after infection. A fortnight before Christmas 
he had peculiar tickling sensations in the face, accompanied by a 
peculiar bad taste in the mouth. Just after Christmas he had 
this curious numbness and tickling in the face again, and on this 
occasion he lost his speech for four hours. An hour and a-half 
after the loss of speech he had a fit, in which he remained un¬ 
conscious for three-quarters of an hour. He does not know what 
happened in the fit, but he did not bite his tongue or pass water. 
Since then he has had a feeling of formication in the right leg and 
numbness, which lasted for fourteen days. He has had no fits 
since. There is no evident facial paresis. The tongue is pro¬ 
truded in the middle line. He walks with a stick and there is a 
little dragging of the right leg; both knee jerks are exaggerated, 
especially the right. He has a good grasp in both hands. There 
is no girdle sensation. Pupils are equal and react to light and to 
accommodation. No ocular paralysis, and there is no appreciable 
loss of sensation to tactile or painful impressions. He has 



suffered with headache, but there is no tenderness on percussion, 
hearing is not impaired ; no ankle clonus. His speech and writing 
are quite natural, and his memory and intellect fair, as shown by 
the answers he gives to questions. No history of fits in the 

Provisional diagnosis. —Gumma of left fissure of Sylvius and 
arteritis, and for this he was ordered anti-syphilitic treatment. 

February 14.—Headache is gone; he has had no fits since; 
he feels much better, and complains of nothing save a feeling 
occasionally of heaviness in the right leg. 

Case 33.— Syphilitic gummatous meningitis, large gummatous mass 
filling left Sylvian fossa, general peri and endarteritis. 
Diagnosed as general paralysis, and after post mortem had 
been made and the above facts recognised still filled up as 
general paralysis. 

L. H., admitted into Claybury, March 1, 1894, aged 47. 
Occupation, porter. 

The following is the medical certificate—Facts indicating 
insanity observed at time of examination : “ Says he has fits, and 
I should think he is epileptic. He is unable to converse, he has 
great difficulty in answering questions and has no clear idea 
where he is or where he was brought from.” 

The present illness commenced four months ago with fits. 
(No history of syphilis or alcohol recorded.—F. W. M.). His 
condition on admission as regards bruises, tongue, &c., is fully 
described and presents no facts of noteworthy interest. He had 
spastic gait and exaggerated knee-jerks. He is said to have a 
full red face showing a lack of expression owing to diminution 
of natural lines. His speech is slurred. He breaks off his sen¬ 
tences and leaves them unfinished, and he is dull and unappre¬ 
ciative. He says he had a fit three years ago, losing his memory 
and speech. He has old facial paralysis of the right side. (There 
is no note made recording headache, nor are the condition of the 
pupils and fundus noted.—F. W. M.) 

April 2.—There is no mental improvement. He has had one 
or two epileptiform convulsions, but is well enough to get up 

May 26.—Unimproved. He is very feeble and demented, and 
dirty in his habits, and needs constant looking after. 

August 27.—Health improved, dementia unchanged. 

January 30, 1895.—He is suffering from general paralysis of 


the insane. Helpless and unable to move about without help. 
Demented and lost; poor condition. 

April 30, 1895.—There is no change to record in his mental 
condition. He cannot speak at all and has to be kept in bed. 
Some paralysis of left arm. (There are no further notes.— 
F. W. M.) 

Died November 30, 1895. Apparent cause of death certified 
general paralysis of the insane. Whether or not ascertained by 
post mortem ?—not yet. 

This was a case which was assumed to be general paralysis, 
although there was a very definite history pointing to brain 
syphilis, in which the cause of death was certified as general 
paralysis, but which the autopsy showed, in a most convincing 
manner, to be due to a general gummatous meningitis and general 
peri- and endarteritis. 

Autopsy .—A large gummatous mass was found occupying the 
left Sylvian fissure, with softening of the surrounding brain sub¬ 
stance. It was undergoing caseation in the middle. The mem¬ 
branes generally were thickened, opaque, and adherent slightly, 
the vessels were thickened, especially those entering into the 
formation of the circle of Willis. The cause of death was attri¬ 
buted to general paralysis. These were the essential facts obtained 
from the notes by Mr. Dudley Cooper, who made the post mortem 
and recorded the facts. 

A careful microscopic examination of the brain and spinal cord 
showed general cerebro-spinal syphilitic meningitis with intense 
universal endarteritis and peri-arteritis (r ide photomicro. 2, p. 38). 
The spinal meningitis did not extend far down the cord, only the 
upper two or three cervical segments being involved; but the 
inflammation of the meninges was very marked about the base of 
the brain, all the vessels being affected by an acute inflammatory 
process, causing thickening of their walls. The larger arteries are 
affected as well as the smaller; in the former the inner coat is 
greatly thickened, but, although the lumen is greatly diminished, 
I could find no obliteration, except in the aforesaid gummatous 
mass, existing in the left Sylvian fissure {vide photomicro. 1, 
p. 38). The endarteritic process has not in the larger vessels 
affected the wall equally ; generally the one side is more affected 
than the other, making the lumen half-moon in shape. In some 
places the elastic lamina of the internal coat is ruptured. There 
is a marked peri-arteritis, and even the muscular coat is infiltrated 
with leucocytes. The small vessels are markedly affected in all 
their coats, being infiltrated with leucocytes and swollen so much 
as to either obliterate the lumen or greatly diminish it. 



There is marked flattening of the spinal cord, due to descend¬ 
ing degeneration and sclerosis in the direct and crossed pyramidal 
tracts, and also, to a less degree, of the antero-lateral regions; 
probably this process commenced at the time of the loss of speech 
and the fit, three years before admission. 

Case 34.— Case of multiple syphilitic gummata. General syphili¬ 
tic arteritis and meningitis. Diagnosed as general paralysis 
during life. Certified in the post-mortem book as having died 
of exhaustion of general paralysis. Careful macroscopical 
and microscopical examination revealed the nature of the 

H. B., aged 42. Admitted into Claybury, November 7, 1890. 
Occupation, engine fitter. 

Notes from the case book. —Facts indicating insanity :—He 
told me that he had a French machine put to his right side and 
then turned up to his mouth when it was inside out. That there 
was a low engine which came down low to a nipple and they 
gave them to the persons. That they were going to start the 
mill outside while he vacantly stared at the clock in the ward. I 
saw him on Friday, the 30th, in Bast India Road gazing at the 
sky and houses and stopping. 

Communicated by his wife, E. B.—Told me that he had been 
out all night and when questioned by her he said that he had 
been out only for an hour. Family history:—Mother was in an 

Condition on admission. —Bruises on right and left arms. 
Scar on right forearm and left forearm and left hand. Scratches 
on neck. Old scar of ulcer on right leg. Slight discolouration of 
left eye. Vaccination marks on right arm. Tongue clean. 
Palate high. Teeth fair. Appetite good. Bowels regular. 
Heart and lungs normal. Sight good. Pupils irregular, do not 
react to light or accommodation. Other senses good. Muscular, 
fair. Reflexes increased. Is demented, is suffering from general 
paralysis. Does not know how long he has been here, how old 
he is, what year it is. Is not depressed or excited. 

November 13, 1896.—He is suffering from melancholia with 
doubtful general paralysis. He is dull, speech is tremulous. He 
has delusions of persecution and rambles about insurance people 
going against him. He has ideas that people put things on to 
him. He wanders aimlessly and his mind is greatly weakened. 


He is wet and dirty in his habits. He is shaky, and his tongue 
is full of fibrillary twitchings. Fairly nourished but health 
impaired. Pupils do not react. Knee-jerks diminished. Was 
admitted with bruises on both arms and left thigh. 

November 20.—Mentally is gradually getting worse. Shows 
no power of recuperation, but is a rapidly progressive case of 
general paralysis. 

November 29. — Getting worse and worse, weaker and 

December 4.—No improvement. 

December 19.—Died. 

Notes from post-mortem book .—Post mortem about six hours 
after death. Body was in cold chamber for three hours. State 
of nutrition—well nourished. Post-mortem rigidity present. 
Discolouration on right leg. Extensive pigmented scars on 
right leg, with old periosteal nodes. Nodes on left tibia. No 
scar on penis. Skull normal. Subdural space contained great 
excess of fluid. Pia arachnoid thickened generally. No adhe¬ 
sions except over central lobes, where they are only slight. 
Sub-arachnoid space fluid slightly in excess. White matter 
small caseous mass size of filbert on middle aspect of brain at 
junction of occipital and temporal lobes. Choroid oystic, very 
granular ventricles. Small softening in left lentioular nucleus. 
There was a diffuse growth pinkish white in colour, hard in 
centre and hard around, involving head of right caudate nucleus 
and grey matter of cortex on right side of inner aspeot of brain 
in front of corpus call. ? gumma. Bronchi—bronchitis. Lungs— 
oedema, hypostasis. Muscular tissue of heart—soft, friable, 
pale, tears easily; slight atheroma of aorta at base. Liver very 
soft and pale, granular. Spleen—large, soft, flabby. Kidneys— 
congested, smooth, capsule strips. Cause of death—exhaustion 
of general paralysis. 


Cause of death .—Multiple gummata, gummatous meningitis, 
extreme syphilitic arteritis of all the basic vessels. 

Upon examination of the brain I found that the growths 
were all syphilitic gummata. That there was extensive basic 
syphilitic meningitis and that all the vessels were affected with 
extreme peri- and endarteritis. These two last-named facts are 
not in the notes. The case had been erroneously diagnosed, but 
this error should have been corrected post mortem. 



Case 35.— Case of multiple syphilitic gummata. Basic meningitis 
and arteritis. History of a chancre and syphilitic infection in 
1894, while in the Army. History of double vision or visual 
affection of some kind in November, 1896. Subsequently 
admission into London Hospital for syphilitic meningitis. 
Then mental symptoms followed necessitating removal to 
infirmary. Admission to Claybury Asylum. Death. Diag¬ 
nosed as general paralysis. 


Out-patient notes. —February 24, 1897.—Staggering for three 
days; worse in the morning. Ptosis of left eyelid six weeks. 
Bheumatism two months ago. Had several attacks. Syphilis 
two years ago. Knee-jerks exaggerated. A. C. marked. Left 
leg a little jerky in walking. No facial paralysis. No weakness 
of arms. Pupils react well. Fundi nil. Urine 1,008. No 
albumen. Diagnosis : Syphilis and chronic alcohol. 

April 28, 1897.—Complete paralysis of left third. Pupils 
dilated; do not react to light or to accommodation. Ptosis. 
Movements in, up and down all absent. Knee-jerks exaggerated. 
Fundi normal. Admitted as an in-patient May 5, 1897. 

Optic discs: edges clean, deep physiological cup. Fundi 
normal Bheumatism eight years ago. Syphilis three years 
ago. Ill four months. Feels no definite pain. Lungs nil. 
Heart nil. Paralysis of left third nerve. A. C. left side. Knee- 
jerks exaggerated. Left eye, pupil dilated. No reaction to light 
or to accommodation. Ptosis. Loss of movement up and down, 
and inwards. Good movement outwards. Crossed diplopia. 

Clerk's notes. —Patient was last at work as a potman in 
November, 1896. Had been at that six months. He was laid 
up in bed for two weeks in November, 1896, with what he believed 
was rheumatism. He had dull pains shooting in the legs and later 
in the arms, especially the right arm. Cannot remember whether 
or not joints were swollen. Did not lose himself. As soon as he 
got up he noticed that he had to hold his head forward and look 
downwards to see straight in front of him. Between November, 
1896, and February, 1897, patient attended Moorfields for six weeks. 
He complains of no pain or headache. He has not been feeling 
himself since November. He used to enjoy reading but does not 
now. He can read type, but things at a little distance seem 
blurred. On February 22, 23 and 24, in the morning, patient had 
a staggering gait, as if he were drunk but he had not been drink¬ 
ing. Patient was in various factories (soap, rubber, Ac.) for short 


periods until five years ago, when he joined the Army Service 
Corps and served three years. Before joining the Corps he used 
to suffer with rheumatism. 

Present illness .—Chancre about three years ago in 1894, 
followed by sore throat and falling out of eyebrows and mous¬ 
tache. Some rash. Had rheumatic fever when a child and 
rheumatic pains from time to time. Family historyFather 
alive, suffers from bronchitis. Mother alive and healthy. Four 
brothers in Navy and three sisters well. No history of family 

Present state .—Well nourished. Eyebrows and moustache 
thin. Much depressed. Somewhat florid expression. Feet cold 
and sweating. Skin of chest: brown pigmentation in round 
patches which have coalesced. There is a scar on left Bide of 
neck caused by boiling lead. Temperature 98°. Ptosis of left 
eyelid. Left pupil dilated. External strabismus of left eye. 
Paralysis of all the movements of eye except outwards, down¬ 
wards, and slightly inwards. Very slight light reflex. Loss of 
reaction with accommodation in left eye. Fundi normal. Diplo¬ 
pia. Respirations 24, quiet, no cough. Lungs and move¬ 
ments symmetrical; resonant on percussion; nothing abnormal 
heard on auscultation. Pulse 72, moderate tension, regular. 
Heart normal. Tongue clean, flabby, slightly indented by teeth. 
Teeth black, appetite good. Bowels costive. No vomiting. No 
headache. Sensation complete, no anaesthesia. Knee-jerks ex¬ 
aggerated. Plantar reflex marked. Ankle clonus very marked 
on left side; present on right side. Sphincters normal. Co¬ 
ordination of hands good, touches tip of nose well with eyes shut. 
Urine, acid. Specific gravity 1022, no albumen or sugar. Slight 
mucous deposit, epithelial ddbris. 

May 7.—Patient’s mother says that he has only been depressed 
for the last fortnight. 

May 13.—Patient does not feel any better. 

Condition of eyes .—Left eye does not react to light. Bight 
eye reacts well. Pupils equal. Left eye reacts slightly to accom¬ 
modation. Bight eye reacts fairly well to accommodation. 
Slight ptosis of left hd. External strabismus of left eye. Left 
internal rectus paralysed. Left eye cannot be moved up or 
down. Paralysis of superior and inferior rectus. Left eye can 
be moved outwards and slightly up and in. Field of vision slightly 
less than normal. Diplopia. Horizontal meridian. Blue glass 
opposite patient's right eye. At extreme left (pts.) of visual field 
one object is seen; on moving to it, just after crossing meridian 
plane of body, two are seen. The images are crossed, the darker 



being to the left; as the object is moved further to the right the 
two objects diverge from one another. Vertical meridian. Glasses 
as above. In the inferior segment one image is seen, in the 
superior left two images appear crossed, the dark image appear¬ 
ing to the left of the other. At the same time the dark image is 
seen below the other, and as the body is moved further up the 
two images diverge from one another. 

May 14.—Left pupil larger than right. 

May 18.—Left pupil smaller than right. More power of 
movement in left internal rectus. Patient is depressed. Does 
not comprehend easily what is said to him. Pupils react to light 
and to accommodation. 

May 19.—Ptosis better. Patient became unmanageable and 
was removed to infirmary. 

House Physician's summary .—Paralysis of third left nerve. 
Ptosis. Dilated fixed pupils. Paralysis of superior, inferior, and 
internal recti. Syphilitic meningitis. Melancholia. Sent to 
infirmary, where he immediately tried to commit suicide. Weight. 
9st. l£lbs., increased to 9st. 21bs. Temperature always between 
97‘2° and 99°. Bowels irregular. I am indebted to Dr. Schor- 
stein for kindly supplying me with the above notes. 

O. W. D., aged 27; occupation, barman; was admitted into 
Claybury Asylum on June 1, 1897, under the following medical 
certificate. The patient has been very depressed since admission, 
very morose, and refuses to answer most questions. Can give no 
intelligent account of himself. Looks at the walls of the ward in 
a vacant manner for some time and begins to cry. Is of suicidal 
tendencies. Says he wants a knife to do away with himself 
before the executioner comes. Has a delusion that he is con¬ 
demned to death and will be hung. Tried in the night to get at 
the knives. 

Family history .—Maternal great-aunt and paternal aunt died 
insane. Served three years in the army and had a fall from a 
horse, hurting his foot. Had rheumatism very badly three times. 
Was reserved and Bteady. 

Mental condition on admission .—Very difficult to examine, as 
he refuses to answer questions. He is apparently demented, pays 
no attention to his surroundings, and as a rule takes no heed 
of what is said to him. He has complained of his head and 
is always sleeping or trying to sleep. Does not take his food 
well, becomes irritable when others make a noise, because he 
says he cannot sleep. He is at times noisy and impulsive. No 
delusions or hallucinations discovered. He is suffering from 
imbecility and melancholia. He is very depressed ; weeps noisily 


without cause. Behaves like a child. Will not answer ques¬ 
tions. Resistive. Strips himself. Is very impulsive. Bushes 
for the windows and requires the constant attention of an 

June 21, 1897.—Is very noisy, troublesome, and exalted, con¬ 
tinually complaining of pain in the head. Very ready and willing 
to fight with his fellow-patients. 

June 28.—Has a delusion that he is wonderfully strong. 

July 28.—Is very much thinner and weaker. Shows no signs 
of improvement. Presents all the signs of general paralysis 

September 28.—Has grown much worse both physically and 

October 5.—Has been in bed for twelve days and had a 
seizure this morning. Died at 8.30. 

Post-mortem notes (by A. T. White).—State of nutrition, poor 
and emaciated. P.M. rigidity marked. No scar on penis. No 
external evidence of syphilis; no bedsore. Middle ear and eye.— 
There was well marked ampullary dilation of the right optic nerve 
at the entrance of the nerve into the eyeball. The dura mater 
was not adherent or thickened. The dura of the posterior fossa 
was pink and congested. Pia arachnoid.—On opening the dura 
there were two raised nodules, one on each side of the longitudinal 
fissure (about the size of Barcelona nuts), situated one over each 
paracentral lobule; they were soft to the touch. The pia was 
thin, dry, smooth, and sticky. The pia was adherent over these 
two patches. The arteries were normal, except for slight thicken¬ 
ing of the right vertebral. The brain weighed 1,230 grms. 
There is a yellowish patch on lower surface of frontal and at 
lower part of left quadrate lobe. It is dry looking and sticky. 
The convolutions were normal except for flattening. The 
areas of cortex and medulla round the growth are deeply con¬ 
gested. The white matter is soft where broken down in pons, 
and round the posterior horn of the lateral ventricle. The 
posterior part of the right lateral ventricle was much softened 
and broken down, white colour. Corpus striatum.— Right 
implicated in a mass of growth. Pons. — A mass of firm 
growth, with secondary haemorrhage involving tegmentum and 
fillet. It is soft and filled with recently extravasated blood, 
and in others filled with growth. The bronchial glands were 
pigmented. There was nothing abnormal in the lungs. The 
heart weighs 270 grms. Aortic valve.—Old endocarditis. Muscu¬ 
lar tissue firm. Liver weighed 1,180 grms. Very congested, 
firm, capsule normal. Spleen weighed 130 grms. Normal, firm. 


Cuae 8f» 

of the base of the brain and arteries exhibited the typical 
appealranees presented by meningitis and .scute arteritis. The 
walls of the arteries were the seat of intense inflammation, 
and there, were new. capillary vessels developed in tho middle' and 
inner coats The left optic nerve, at its entrance to the eyeball, 
showed an ampullar) swelling, and microscopies! examination 
of the retina showed numerous haemorrhaget?, but I could Slid 
no endarteritis. 

102 ' ' 


Kidneys; right weighs. 1.42 grins., left 131. Cortex not wasted 
or .adheteiih- Very congested. Bladder distended. Testicles 
weigh s.eventyrfo.trr grass. 

Cause of 'kath ..—Multiple gdmrasta. Syphilitic meningitis 
and artentis. Portions of hraiti and pons kept. Eyes removed 
lor exaniinatioo C- Microscopical examination of the tumours in 

’ .v: p/,?' r '. £ 'V'v’.i- fv. »vi/;V4 *\vvv .<-’K ‘Yj'-’v ’• 

.\;y',',!$| •;|;Y'>‘Jy ; ; f. .V f . 


Case 36.— Gummatous meningo-encephalitis involving Broca’s con¬ 
volution and the lower portion of the ascending fronted and 
parietal convolutions. Progressive speech defect and dementia. 
Bight facial paresis. 

W. B. C., aged 64, clerk, admitted into Claybury on Sep¬ 
tember 8, 1897. 

Notes from case book. —He says he will never die and does 
not know what he is or where he is. He regards with amaze¬ 
ment a common chair and cannot imagine it possible that human 
hands made it. Suddenly he bursts into laughter for no apparent 
cause. Has a delusion that his wife is starving. 

Condition on admission. — Small sebaceous cyst on head. 
Facial paresis on right side. Is unable to whistle. Pupils equal 
and regular, and react to both light and to accommodation. He 
has a scar on groin. Urine 1,020 acid. No albumen. Phos¬ 
phates. Pulse 88; small, regular. Knee - jerks increased. 
Speech slurred and stumbling. Was born and always lived 
in London. It is impossible to make anything out of his 
history as he is utterly demented. He cannot answer the 
simplest questions with any intelligence. Is somewhat exalted. 
Has a very peculiar stumbling speech, which is very indistinot, 
but not like that of a general paralytic. He has great loss of 
memory for recent events. Has no idea how long he has been here, 
or what day of the week it is. Incoherent. He is suffering from 
dementia, secondary to mania. Is quite lost to time and place. 
He gets so excited at times as to feint an epileptic seizure, then 
he becomes tearful, sighing and asking what is to be done. He 
is restive, wet and dirty, looks restless and vacant. It is difficult 
to get any coherent answers from him. In impaired health and 
condition.—B. J. 

September 20, 1897.—He has been very noisy, laughing and 
crying without cause, at times seemed depressed, accusing 
attendants of robbing him and poisoning his food. Sometimes 
incoherent, at times says that he wants to die and that he would 
cut bis throat. Wet and dirty. 

September 27. —Got more feeble, but remains noisy and 

October 5.—Speech got worse, being able to say “ yes ” and 
“ no ” but no other words. Used to mutter a good deal to him¬ 
self. Always wet and dirty; gradually more demented. 

November 5.—Had difficulty in getting him to take his food. 

November 25.—Died without any material change taking 
place except combined feebleness and exhaustion. 



Post-mortem, notes. —Post-mortem nine and a-half hours after 
death. Fairly nourished state of nutrition. Post - mortem 
rigidity marked. Skull.—On the inner side tough and eroded 
over ascending frontal and parietal convolutions. Dura mater. 
—Thickened and adherent both to brain, and in places to skull 
where the bone was thickened. Pia arachnoid congested. The 
brain was wasted, convolutions wasted, sulci broad and deep, 
weighed 1,210 grins. White matter congested. There was a 
firm white growth adherent to the membranes and situated in 
base of the left ascending and third frontal, and encroaching on 
the ascending left parietal convolutions. Not encapsuled. 
Bight pleura.—Recent lymph. Lungs both congested hypo- 
statically, right more than left. Bight lung, lower lobe, disinte¬ 
grating at base. Heart weighed 280 grms. Muscular tissue right 
side dilated. Blood clot. Slight patches of atheroma at base 
of aorta. Liver 1,250 grms. Scar on left lobe of liver. Omentum 
adherent to upper surface of liver. Spleen weighed 200 grms. 
Bather large and somewhat soft. Bight kidney 153 grms., larger 
than left and congested. Capsule strips easily. Cortex not 
much diminished in size. Left kidney 205 grms. 

Microscopic examination of the portion of brain affected 
showed fibrous thickening of the dura mater with very thick 
walled vessels. Thickening of the pia arachnoid and extending 
from this along the vessels a round-celled infiltration extremely 
vascular, the arteries with very thick walls and many with their 
lumen obliterated. In one part of the neoplasm the cellular 
infiltration stains very imperfectly and is obviously undergoing 
regressive metamorphosis. 

Cause of death. —Hypostatic pneumonia and localised gum¬ 
matous meningo-encephalitis. 

Case 37.— Case of cerebral softening in a man the subject of 
syphilis, hemiplegia and epileptiform convulsions. Post¬ 
mortem : general arteritis cerebri, endocarditis ; death from 
thrombosis of the basilar artery. 

C. B., aged 45, dock labourer, admitted into Claybury 
Asylum on June 8, 1897, under the following medical certifi¬ 
cates :— 

Patient is in a dazed condition and will not speak intelligibly, 
but answers “ yes " to whatever is said to him. 

Patient’s wife states that patient had an injury to his head 
six years ago. Since that he has always been bad in his head. 


Two years ago he began to have fits. A year ago he became 
paralysed on right side and lost his speech. He has been 
strange and childish since then. 

Patient has been married 26 years, has five children alive, 
and three dead. The youngest is 13 years. Patient was born 
in Ipswich and has lived in London for 27 years. 

Condition on admission .—Pigmented syphilitic scars on left 
leg. Slightly enlarged inguinal glands. Small penile scar. 
Tongue clean, cannot protrude it. Heart very irregular, murmur 
cannot be detected. Pulse 100, very irregular. Lungs normal. 
Pupils equal, regular; react to light and to accommodation. 
Muscular fair. Reflexes, right much increased, left slightly so. 
Has right hemiplegia and motor aphasia. Bowels constipated, 
palate normal, teeth fair. Urine contains albumen. He cannot 
speak sufficiently distinctly to be understood. He is apparently 
demented. Takes no interest in his surroundings but sits still 
in the wheel chair or lies in bed quietly and without making any 
attempt to speak. Occasionally restless at night. Has severe 
epileptic fits. He is wet but not dirty. Understands apparently 
when spoken to.—H. W. L. 

June 15, 1897. — He is suffering from post hemiplegic 
dementia. He mutters incoherently to himself. Stupid in 
appearance. Does not appear to realise what is said to him. 
He is wet and dirty in his habits at times. He has had three 
epileptform convulsions since admission. He has to have every¬ 
thing dono for him. He is fairly nourished but in impaired 
health from right hemiplegia.—T. E. E. S. 

Nothing noteworthy stated until August 10, when the 
following note was made. He had a typical epileptic fill with 
tonic and clonic convulsions in my presence recently.—A. T. W. 

September 25.—He is in bed with diarrhoea and mucus in 
his stools. There has been a little blood at times. His heart 
is exceedingly irregular and he has dilatation of his heart. 
There is a trace of albumen in his urine.—A. T. W. 

September 29.—He is to-day semi-conscious. He had three 
fits. Does not move or take any notice when spoken to. His 
diarrhoea is better. His pulse is still most irregular. There is 
no fresh paralysis. His pupils are equal and re-act to light and 
to accommodation. Knee-jerks are exaggerated, the right more 
than the left. Cannot protrude his tongue.—A. T. W. 

October 1.—To-day he was much worse, the coma being more 
profound. Heart very irregular, with cantering action. No 
murmur audible. The diarrhoea has practically ceased. He died 
at 11.25 a.m.—A. T. W. 



Post-mortem notes. —Post-mortem about twenty-four hours 
after death. Body well nourished. Post-mortem rigidity passing 
off. Tattoo marks on right forearm. Several bedsores. Scar 
on penis. Pigmented scars on front of both tibiae. Both 
middle ears normal. Dura mater normal. Subdural space 
increase of fluid. Pia arachnoid thickened, gelatinous; not 
adherent, not opaque. Subarachnoid space contained a con¬ 
siderable excess of fluid. Patches of nodular atheroma on 
oerebral vessels. Basilar was blocked by thrombosis. The 
general appearance of the brain was wasted, watery, and soft. 
The cerebrum was symmetrical. There was a patch of soften¬ 
ing at the apex of the left temporo-sphenoidal lobe. Brain 
reserved for further examination, and after hardening in 
formalin patches of softening were found in the left centrum 
ovale involving the fibres of the corona radiata and the anterior 
half of the internal capsule. The right pleura was normal and 
the left pleura old adhesions. The lungs were congested and 
oedematous. There was increase of fibrous tissue especially 
around bronchi and bronchioles. The pericardium was thickened 
and generally adherent. Heart, pulmonary valve and tricuspid 
both normal. Aortic valve, recent vegetations. Mitral valve 
greatly thickened; also several patches of recent vegetation. 
The right ventricle and auricle were much dilated and the 
walls were thin. The left ventricle was dilated but the wall 
was about the normal thickness, substance firm. Left auricle 
very dilated. Coronary arteries patent. Atberoma of aorta. 
Weight 465 grms. The liver weighed 1,900 grms., was fatty, 
cirrhotic (alcoholic) and very pale; large, no soars. Gall 
bladdder distended but contained no stones. The spleen 
weighed 150 grms. The capsule was thickened and firmly 
adherent to diaphragm; a large milk patch about the size of a 
half-penny; substance firm. The kidneys were pale and greasy. 
The capsule was non-adherent, but the surface was irregular. 
Old infarctions converted into fibrous tissue. Weight, right 182 
grms., left 213 grms. There were patches of congestion, but no 
ulceration of the small intestine. Large intestine: small 
punched out ulcers all along large intestine; most of the 
ulcers were extremely minute, not much larger than pin heads, 
others about six times this size. Patches of congestion. 
Colitis. Cause of death—ulcerative colitis, thrombosis of basilar 
artery and morbus cordis. 

Microscopial examination of the spinal cord showed degenera¬ 
tion of the right crossed pyramidal system and the left direct. 
Examination of the cerebral arteries showed nodular atheroma 


(of syphilitic origin probably). The basilar artery was blocked 
by a recent organising thrombus, not of embolic origin. The 
coagulation of the blood in this vessel was probably produced 
three days before death; but the notes do not indicate clearly 
the onset of the thrombosis. It was in all probability induced 
by the slowing of the circulation in a diseased vessel; the 
weak acting heart and the exhaustion produced by the colitis 
materially contributing to the slowing of the blood stream. 

It is possible that the softening may have been due to 
multiple embolism from the diseased valves, but the notes do 
not state whether the onset was sudden or gradual. 

F. W. M. 

Case 38.— Universal syphilitic arteritis. Chorio-retinitis, old 
iritis, and other signs of syphilis. Diagnosis : general paralysis. 
Post-mortem called general paralysis. 

J. J., aged 46, labourer, admitted into Claybury in May, 1893; 
died February, 1897. Had been married for twenty-five years. 

The following is the medical certificate under which he was 
admitted :—Rambling in his talk; excitable in his manner. Says 
his wife is being confined of a boy, which is contrary to fact. 
His conversation is bordering on indecent. His stepson states 
that his father has abused himself before his wife and in the 
presence of his children, that he has exposed his person to women 
in the common washhouse, and that he has used threatening 
language to his wife. 

His present attack commenced eighteen months ago, when he 
had a fit and foamed at the mouth whilst at work. He slept 
badly, his appetite was bad and he lost flesh. His moral character 
altered and he became irritable and indecent in his behaviour and 
dirty in his habits. 

Condition on admission. —Pigmentation and old ulceration of 
left leg. Tongue tremulous, moist, furred; palate normal; 
teeth fair. Appetite good; bowels regular; viscera normal; 
urine normal. Heart: H. A. B. fifth space sounds normal. 
Pulse 80; regular; tension moderate. Lungs: emphysema, 
otherwise normal. Sight fair in right eye; none in left. Old 
leucoma from traumatism in childhood. Right pupil reacted 
slightly. Hearing, smell and taste fair. Muscular, average 
power. Gait fair. Reflexes present, deep and superficial. 

Mental condition. —He is a general paralytic. His speech, 
reaction to questions and attention are fair. His memory for 
recent events is impaired, but for remote events is fair. He is 



slightly incoherent and has no illusions or hallucinations at 
present. He has a feeling of well-being. Is better than ever he 
was in bis life. Can lift five cwt., &c. Thinks Christ lifted him 
from his knees when he was in church. He is not impulsive, 
and denies that he exposed himself to women. He is not 
suicidal.—Ernest Wills. 

Patient was in Hoxton House twelve months ago because 
he was not very well. 

A well-nourished, well-built man, with whiskers shaved off and 
wearing a dark-brown beard and moustache turning grey. Has an 
opacity of left eye. He chats freely and gives his history fairly 
coherently. Talks rationally of his wife and family, but there is 
a marked wanting in the fitness of things. He says he does not 
mind lecturing to anybody on the anatomy of the human body or 
on any matters relating to theology or divinity. Exaltation indi¬ 
cative of g. p.—R. Jones. 

No further noteworthy facts stated until the following note 
was made by Dr. Jones. 

May 1,1894.—He is suffering from mania of general paralysis. 
He is deluded about his power to preach, work, lecture, <fcc. He 
is blind in one eye. He is well-nourished, but weakened from 
general paralysis. 

August 21.—He has the tremor and slurred speech of g. p.— 
E. Wills. 

April 13, 1895.—He is suffering from dementia after general 
paralysis. He is somewhat feeble; has had several seizures. 
He is at times excited and violent so far as his violence can 
extend with paralysis. He talks to imaginary persons and is also 
at times very restless. In fair health and condition.—R. Jones. 

October 15.—He has had a few slight seizures. There has 
been no change in his mental condition, which is that of advanced 
dementia.—C. D. Cooper. 

January 19, 1896.—He is now oonfined in bed in the in¬ 
firmary and is having universal seizures.—C. D. Cooper. 

February 18.—He died this day of exhaustion of general 
paralysis.—C. D. Cooper. 

Post-mortem notes. —Post-mortem about twenty-four hours 
after death. Body poorly nourished. Post-mortem rigidity 
present throughout. Two large gangrenous bedsores on sacrum 
about 2£ inches in diameter. Small sore on left hip. Large 
ulcer on both legs. Numerous symmetrical pigmented scars on 
legs and body. Skull symmetrical; fair thickness; dense; con¬ 
gested. Dura mater thickened and adherent to the calvarium in 
the frontal region and at the apex. Subdural space contained an 


igiiims pt fluid. K» arachnoid opaque ; thickened. Adherent in 
small patches over the frontal and motor areas, Subarachnoid 
space contained excess qf fluid. Thera was nodular atheroma of 
vessels of 'eircls of Willis. Weight, 4? ounce*. Weight pf right 
hmdijBiph«fe. ounces; weight of left ; hemisphere* 10| ounces; 
right pbuira,, old adhesions at apes:: bit pleura, normal. Bronchi 
and bronchial glands normaL Bight 1 nog weighs 30 ounces ; 
solid tndeina and some congestion of lower lobealight congestion 
of iippek amd. middte. \2feflf lung weighed '23 uttocesoedema and 
eOngeaftioa of base, but not $q inarked as on the right side, 
Pericardium normal. Heart-: pulmonary; valve normal; tricuspid 
Mcu oKtl. Aortic valve, rigid ; shrivelfed ■; incompeteutv Mitral 
valve thiekeaed ; patches of atheroma. Weight, 71 ounces, 
fi&toe Soft ,' pale ;• fatty,. Coronary %^tfefcv&tlwro- 
toatotu*. Aorta atheroma toUs; : ttoe<? largo plates to first part 
of aorta, oho ulcerating. Liver weighed 43 ouncef j soft ; flohhy. 
Gall bladder uormai. gpfeett weighed 5 ppuces. Kidneyti 
weighed. 5 k pi to oee each; Capsule, ’^dlie^en.fiy.'Cprtex wasted', 
congested. Bladder cob wanted and empty. CauWa of death - - 
genera}, paralysis. Aortic and mitral disease.—T. E, K. S. 


PuoTOMJcaue r« vr h S>. 

Trwoverae section of vertebral. basilar, ;m<l middle cerebral ark'rj.oK. 
yhovyitigoM fibrous cicatricial syphilitic undartenti*. Typical halbutoou 
churactcy . The ^rteid* 1 . <it the brain shovyed a much m»t« 

eudaftofith, yhigaiStAtiou a diameters. 



Microscopical examination showed nodular atheroma of the 
larger vessels of the circle of Willis. Fatty change in the deeper 
layers of the much thickened intima, otherwise it had an appear¬ 
ance like old scar tissue. The small vessels, however, were not 
atheromatous, and some of the sections of the opto-striate vessels 
were quite characteristic of endarteritis syphilitica. 

Examination of the cortex cerebri showed the tangenital 
system of fibres had undergone no appreciable atrophy, and I 
regard this as absolute proof that it was not a case of true 
general paralysis. 

Case 39.— Multiple syphilitic gummata. Endarteritis, periarteritis 
and basic meningitis. Brain disease in the form of left hemi¬ 
plegia occurred eight months after infection and progressed 
rapidly. Mercury and iodide in only moderate doses for a 
few weeks while under treatment. Death, Hanwell asylum 
twenty months after onset. 


W. R., aged 26, occupation painter, came to the out-patient 
department, under the care of my colleague Dr. C. E. Beevor, 
on January 30, 1894. He complained of slight weakness on 
shrugging the shoulders and on raising the arm. There was a 
history of partial left hemiplegia since the first week of October, 

He gave a history of having contracted syphilis in February, 
1893; the possibility of syphilis as the cause of the nervous 
manifestations therefore suggested itself. He was advised to 
take 15 grains of pot. iodide with 1 drm. of the liq. hydgrag. 
perchl. three times a day. 

When I took over Dr. Beevor’s patients a few weeks later I 
find that I wrote the word lues ? against this date, but there is 
no evidence in Dr. Beevor’s hand-writing, although the prescrip¬ 
tion shows what he thought. This treatment was continued 
until February 13, when the doBe of the drugs mentioned above 
was diminished by half. 

February 27, 1894.— Twice within an hour yesterday he 
stammered and stuttered, and could not do more than mumble. 
Each attack lasted ten minutes. During the attack he suffered 
numbness and tingling in the limbs, chiefly in the right hand, 
but in the hands more than in the legs. Grasp in the hands 
good and equal. Knee-jerks brisk. He says that two months 


ago the right leg gave way under him. The treatment mentioned 
was continued through this period. 

March 2.—Admitted into the hospital. 

March 13.—fate was back in the out-patient department, when 
treatment with iodide of potassium and liq. hydrag. perchlor. was 
continued. The doses of these drugs do not seem to have been 
large (10 grains of the first and about 30 min. of the latter, three 
times a day). 

April 10.—Vision of the right eye diminished. Pupils react, 
cannot count fingers. 

May 1.—Pain in right side of face and neck. Treatment in 
the meantime was continuing as before. In addition he was 
having doses of sulphonal at night. 

May 22.—Almost complete absence of vision in the right eye. 
He can detect light faintly. Pupil inactive to light. Slightly 
active to accommodation. Indistinctness of upper margin of the 
disc. No optio neuritis in the right eye. 

Treatment was continued, with the exception that I slightly 
increased the doses of hydrarg. 

August 17.—He has had a severe fit, which his mother says 
was “ jerking ” in character, and lasted over one hour, leaving the 
patient very dazed. He says he had no warning of the fit, and 
did not know that he had a fit until next morning. Mother says 
that he was very peculiar for two days before. He “ frothed ” 
at the mouth. 

The following description of the fit was got from an eye¬ 
witness :—First noticed the forearms jerking, and saw the 
patient falling. Caught him and laid him on the floor. Noticed 
that all the limbs were jerking irregularly. The head was 
thrown up from the floor irregularly. There was foaming at 
the mouth. He was unconscious for an hoar after the fit, 
and was more than a week in getting back to his normal 
condition of health. 

Treatment .—15 gras, of pot. brom. were prescribed for him 
twice a day. 

August 24.—Optic nerves: right, on the upper part there 
appears to be a certain amount of swelling reaching down to the 
entrance of the vessels. The vessels themselves seem to be eeen 
through a haze. Left, upper margin brick red in colour. Veins 
very distinctly seen, and they dip suddenly into the lamina 
cribrosa. Treatment by mercury and iodide was once more 
adopted, the amount being 5 grns. of the iodide of potash, and 
1 drm. of the liq. hydrarg. perchlor. He had also occasional 
courses of potassium bromide. 



October 19, 1895. — Development of mental disturbances. 
Loss of temper, moroseness, excitement. No evidence of delu¬ 
sions. On account of these symptoms he was admitted to the 
Han well lunatio asylum. 

W. G. R., aged 27. Admitted into Hanwell asylum, October 
13, 1894. 

Medical certificate on admission. —Brought to Hanwell as a 
lunatio found wandering at large. He behaves in a very strange 
manner. Talks incoherently to himself. When asked questions 
he only remarks, “ Thank you, sir,” “ Good morning,” and these 
are the only words he uses. He shouts, is restless, and beyond 

History of the case obtained from brother. —Nationality Eng¬ 
lish. Education fair. Occupation cheesemonger’s assistant. 

Family history. —Mother has been paralysed for five years, 
latterly bas been rather better, and able to get about. She is 
subject to hysterics. Father most intemperate. 

Personal history. —Not backward as a child, was born at full 
time. Temperate and of sober disposition. Syphilis contracted 
twenty months ago. Neglected it in early stages. Was obliged 
to leave his employment, and he worried a great deal about it. 
He got a little better for a short time, and was thinking of going 
back to work when the symptoms reappeared. This appeared to 
have a very depressing effect on him, and he quite suddenly, three 
months ago, had a fit, followed soon afterwards by a very severe 
one, which left him dazed, dull, and stupid. He wandered out 
of the house and was taken charge of by the police, being unable 
to take care of himself. 

Condition on admission. —Scars on left arm and back, fairly 
nourished, tongue clean, pupils widely dilated, right larger than 
left. Scars of syphilitic ulceration on various parts of body. 

Mental state. —Demented, stares about, cannot speak or 
answer questions. 

October 19.—Imbecile and incoherent, subject to epileptiform 

November 5.—Dull and complains of great pains in the head. 
He says that it was constant. Sight of right eye leaving him. 
Ptosis marked of right eye. 

November 19.—Tremor and inco-ordination of tongue and 
face muscles. Dementia increasing. 

December 4.—No improvement. Has had an epileptiform 

January 2, 1895.—More demented. He has transient attacks 


of paralysis. At present confined to bed owing to paralysis of 
left side. 

February 5.—He complains of intense pains in his head and 
paralysis becoming more marked (treated all through with iodide 
and mercury). He has complete ptosis of right eye. 

June 24.—No improvement. 

September 1.—Utterly demented and is very restless and 
dirty in his habits. He is losing flesh, and paralysis is more 

September 19.—Same. 

February, 1896.—Advanced paralysis, bilateral. 

February 29.—Epileptiform convulsions of left side. 

March 2.—Quite comatose, slight irregular twitchings. Con¬ 
junctivas insensible. Coma. Death March 3. 

Post-mortem notes. — Autopsy March 4, 1896. Pigmented 
scars on legs arm and trunk. Scar on glans penis. There is a 
large projection on the vertex of the skull. On removal of the 
skull cap this was seen to be connected with the dura mater 
and with a large gummatous mass situated at the top of the 
central convolutions about the size of a hen’s egg. The gum¬ 
matous mass had apparently commenced in the membranes and 
grown downward into the brain and upward through the skull. 
On removing the brain gummatous masses were found in various 
situations, viz.: the anterior part of the left temporal lobe filling 
up the adjoining Sylvian fissure and involving Broca’s convolu¬ 
tion. Another gummatous mass involved the left optic tract, 
and the whole base of the brain was the seat of a diffused 
gelatinous greyish white superficial gummatous deposit giving 
rise to a basic meningitis involving all the cranial nerves. On 
cutting up the brain, patches of softening were found in the 
internal capsule on both sides and the crura cerebri on both 
sides, occupying the pyramidal systems. There was endarteritis 
of the vessels seen on transverse section. The heart was fatty, 
the kidneys fatty, and the liver slightly fatty. No atheroma 
of the aorta was found. Several gummatous masses were found 
in the liver and in the lungs. The apex of the right lung was 
adherent and there was an old scar. 

Microscopical notes .—Multiple syphilitic gummata. Atrophy 
of the pyramidal cells. Swelling and breaking off of the pro¬ 
cesses. Stained by Nissl method. The cells appear very faint, 
the sides curved outward, the processes broken off. Great num¬ 
bers of basophile phagocytes are seen stained deep blue around 
the vessels. Cells seen in all stages of degeneration and closely 




resembling general paralysis. Stained by Weigert iron method, it 
is seen that there is a great distension of the perineuronal spaces. 
This statement only applies to the region in the neighbourhood 
of the gummatous deposits and infiltrations. After hardening 
in Muller’s fluid there was naked eye degeneration in both 
pyramidal tracts of the cord on both sides. Apparently vessels 
about the base blocked with endarteritis. The surmise that 
vessels of base are diseased is correct, as microscopical examina¬ 
tion exhibits in the basilar artery a great thickening of the inner 
coat on one side, and the existence of an organised thrombus 
which partially fills the lumen of the vessel. There is well- 
marked degeneration of the pyramidal tracts throughout their 
course in the pons medulla and cord ; but the fillet and posterior 
column are intact. Sections through the island of Beil, Broca and 
tip of temporo-sphenoidal convolutions on the side where one 
naked eye gummatous mass was situated. Examination showed 
a marked thickening of the endarterium of the arteries great and 
small, with complete destruction of the muscular coat by the 
round cell infiltration, the crinkled elastic coat being the only 
means of recognising in some of the sections that arteries were 
present, as the lumen is completely blocked. In sections a little 
further removed from the gummatous mass the lumen although 
greatly diminished is present, but the muscular coat is destroyed 
by the neoplastic formation. These sections seem to show that 
the gummatous process begins in the perivascular sheath. 

Case 40.— Case of brain syphilis. Universal arteritis. Basic 
gummatous meningitis extending into both Sylvian fossa. 
Ependymal gummata of lateral ventricles. Extension of 
meningitis to spinal membranes. Notice of death given as 
general paralysis and pneumonia, although the notes and 
treatment distinctly indicate that it was a case of brain 

J. McK., single, aged 42, occupation, seaman. Admitted 
into Claybury, September 28, 1898. Cause of insanity, syphilis. 
The medicai certificate states that he is dazed, dull, stupid, and 
childish. He talks incoherently and seems mentally lost. No 
history was obtainable from him, and he had no friends. Tattoo 
marks on the right arm and various old scars on the left elbow 
forearm, little finger of the right hand, large ulcer on the 
sternum. Ulcer to the left of the umbilicus. Ulceration of the 
right nostril. Heart normal. Lungs normal. Pupils unequal, 


right 5£ mm., left 4 mm., fixed to light and to accommodation. 
Slight ptosis of right eye. Muscular fair. Walk, gait paretic, 
shuffling. Tremor of hands. Reflexes greatly exaggerated. 
Handwriting unable. Mental.—He is grossly demented, and 
cannot answer the simplest questions but occasionally he will 
mutter some incoherent nonsense. He is very untidy in his 
dress and appearance. Is utterly lost and dazed. Has to be led 
about wherever he goes. He has several ulcers about him which 
are of a tertiary specific origin. Syphilis being also the cause of 
his insanity.—F. P. P. 

He is the subject of dementia. He is unable to grasp the 
meaning of the most simple questions but mumbles and rambles 
along in an incoherent manner. Has no idea of time or place. 
He is in impaired health but is fairly well nourished. Ulcer on 
right nostril.—C. T. E. 

October 10.—Dull and confused in his ideas. He has no 
memory and cannot give his history. He has a sore on abdo¬ 
men, and left little finger seems to have been crushed before 
admission. Intellect much impaired and he has some appearance 
of chronic renal disease, not unlike myxcedema. Rather helpless 
and of defective habits.—R. J. 

October 17.—Under anti-syphilitics the ulceration on his 
abdomen and the node on sternum have almost entirely dis¬ 
appeared. He is certainly less dull. Will answer simple ques¬ 
tions, but the improvement is not very marked. 

October 24.—He continues to improve slightly under full 
doses of iodide of potassium, both mentally and physically. 
—F. P. P. 

Died—December 9, 1898. 

Post-mortem notes .—Post mortem about sixty-five hours after 
death. Body was suspended in the cold room. Considerable 
superficial fat, bright yellow. Post-mortem rigidity not present, 
but body stiff from cold. Evidence of syphilis. Absence of 
frsenum. Scar on penis. A scar, with an irregular serpiginous 
edge and papery, on right of abdomen. Scar on left side of nose. 
Scar on left forearm. Scar on right shin ; brown and pigmented. 
Stricture of meatus. Skull symmetrical, thick and heavy. 
Pupils: right, 5} mm.; left, 4 mm. Right ptosis; not noted 
during life. Membranes : no adhesions, no thickening. Subdural 
space free of fluid. The whole floor of the interpeduncular space 
is covered with a layer of gelatinous-looking lymph. This extends 
up each side of the middle cerebral artery into the Sylvian fissure, 
especially of the left side. After hardening in formaline solu¬ 
tion, transverse section of the Sylvian fissure showed markedly 

,'i it? . ABCHI VKS 

1 . . 

thickened vessels lying iu t he gumma tems tissue. .Slight thicken¬ 
ing, nodular. of basilar ftb.d vertebra! arteries (microscopical 
dSBiroftiiticiu tb be inadph -. Oritjev^l a^jpeatranoe of bwiiii; firm. 
CWrbbruVii seems ^'r»BjVftVribs,L Bight ^tnlspl^lrcs'iinij^pt!. $$$ 
grrris.: left hemHphere weighs 60;V grms Convolutions- look 
normal. a-xcept slight .genera! tl'aWeeing. Fia stiripe vefrtdily from 
cortex. Both lateral Voutficles diluted, but no granulation : on 
the outer eapeet in the white nie-ttet; there tire gelatinous, grey, 
raised rkiduf^ii, yarvuts in size froiit a pea. to a heau. The left 

I’HcnOonuru C. 

Case 40. Section threueh the n'gbt heinCpbere to exposi} lire -huier 
ttupaet of tbo lateral ventricle, (tarn tbo wa!! of v.hicij s;*a be s-t-en maulr-e- 
ti! littlepbaAike swellings. fifeilojcerl oenriy imo* third-. - 

ventricle is ameh more dilated thaiithe .rightsand..on 
the outer Avail of this aide are larger and tporo ptitnevous y^art oh 
pi| right side {hide photo fit. Corpus striatum seeing uorural. 
On the loft side-there is a patch of softening, t he siae of a sixpence, 
m the upper part of the thalamus, and extending into t he corona 
riidiatu. iPoUrfih .ventricle slightly dilated i no ependymal gnihti- 
Jktihjt*' Weight of cereliaUum, port*,' and medulla;, 180 gi.tns,, 
nonimf. Thyroid, normal ; ribs, normal Bight and left pleura 
free from adhesions, but thfere are scattered sinali petechia* on the 


pleurie. Bronchi and bronchial glanda normal. Bight lung 
crepitant, slight hypostatic congestion, no consolidation, 
emphysema of apex and edges, floats in water, weight 550 
grms. Left lung, crepitant, same as right; a few adhesions at 
base. Weight, 500 grms. The heart valves are normal, except 
the mitral, which is somewhat thickened, but competent. Left 
ventricle, 13 mm. Bight side full of dark blood. Coronaries 
patent; weight, 260 grms. Aorta, commencing atheroma. Omen¬ 
tum, considerable omental fat. Liver weighs 1,395 grms.; 
round edged, fatty, some induration. Gall bladder normal. 
Spleen soft, dark, weighs 113 grms. Left kidney, capsule strips, 
surface smooth, cortex fatty, 10 mm., whole organ pale, weight 
153 grms. Bight kidney same as left; weight 150 grms. Large 
intestine; in. the transverse colon there is a large patch of 
thickened mucous membrane covered with little bright red 
petechial elevations, probably commencing colitis. Cause of 
death—syphilitic brain disease and acute colitis. 

Microscopical notes .—Examination of brain.— Sections cut in 
celloidin after being hardened in formol and Miiller. The gum¬ 
matous deposit around the vessels of the left Sylvian fissure, 
stained with logwood and eosin. Under a magnification of 20 
diameters the tissues appear to consist of a delicate network 
infiltrated with cells, in the midst of which are diseased vessels. 
All the larger vessels show very much thickened walls and owing 
to the round-celled infiltration of them, the different coats cannot 
be made out in many of them. Every vessel is affected by an 
obliterative inflammation of the inner coat, considerably dimin¬ 
ishing the lumen of the larger ones and completely, or almost 
completely, blocking the lumen of the small and middle sized 
arteries. Begressive metamorphosis is taking place in the 
endarteritic tissue, similar in character to that of the surrounding 
gummatous tissue. In most cases the infiltration with cells is 
so intense that neither muscular nor elastic tissue elements can 
be recognised in the walls of the arteries. In one vessel the 
middle coat can be recognised by its taking the eosin stain, no 
doubt due to coagulation necrosis of the muscle fibres. Some of 
the small vessels are filled with a thrombus. The adjacent 
brain substance, e.g., the island of Beil, the lower end of the 
ascending frontal and the third frontal convolutions show round- 
celled infiltration and the perivascular sheaths of the vessels 
filled with deeply staining round cells. The farther we get from 
the fissure the less intense this process appears; whereas near 
the fissure of Sylvius the process is so intense that all the 
lymphatic sheaths are blocked by the round-celled infiltration. 



The gummatous encephalitis appears then to be merely an 
extension of the process from the fissure. The vessels of the 
circle of Willis show periarteritis and endateritis, but not nearly 
so intense as in the situation above described, and apparently of 
less recent origin. The right Sylvian fissure was affected by a 
similar gummatous process to the left, but of a less intense 

Sections of the ependymal gummata of the lateral ventricles 
(vide photo 6, p. 116); stained by Nissl and logwood and eosin. 
An elevation the size of a pea, with adjacent tissue, was cut in 
paraffin and examined. All the vessels, great and small, in the 
basal ganglia showed congestive and acute inflammatory pro¬ 
cesses, affecting their walls, starting from the periphery, where 
the process was very intense; the round-celled infiltration ex¬ 
tended into the coats of the vessels, but I did not find any that 
showed an obliterative endarteritis. The round cells covering the 
wall externally in no way differ in appearance nor in staining 
reaction from the leucocytes in the blood contained in the 
vessels, and the process is therefore an acute inflammatory pro¬ 
cess. Where the swelling exists the round-celled infiltration is 
abundant, not only around the vessels of all sizes, but in the 
tissues. No regressive phenomena are found as a rule, the pro¬ 
cess being still in the acute stage. Here and there, in some 
sections, there are small, mostly mioroscopic, particles of necrosis, 
due to softening. The determining cause of these swellings in the 
walls and floor of the lateral ventricles is an acute inflammatory 
process, which, primarily starting in the fissure of Sylvius, has 
spread along the lymphatic sheaths of the lenticulo striate vessels, 
the elevations being due to the process spreading with greater 
rapidity and intensity along some terminal branches of these 
vessels than others. The capillaries in these areas are sur¬ 
rounded by immense numbers of round cells ; in other instances 
not. Spinal cord stained by Nissl method. Sections cut in 
paraffin. Cervical enlargement. All the pia arachnoid mem¬ 
brane shows an acute inflammatory process, infiltration with 
leucocytes and swelling, also periphlebitis and periarteritis. 
Moreover, the inflammatory prooess is spreading from without 
inwards along the septa of the cord. Some of the anterior roots 
show the same process in a very intense degree (vide photo-micro., 
p. 135). Here, again, it is along the perivascular lymphatics the 
process is advancing. Dorsal region and lumbo-sacral also show 
exactly the same appearances, inflammation, but of variable 
intensity, affecting the whole of the pia arachnoid membrane, the 
pial septa, and the anterior and posterior roots. Occasionally 


the periarteritis and periphlebitis has spread to the grey matter 
of the anterior horns. 

Case 41.— Certified as mania; post-mortem turned out to be 
syphilitic brain disease. General endarteritis ; softening in 
both frontal lobes. Healed aneurism of basilar artery. Old 
syphilitic scars on the penis and body. History of alcoholism. 
Illness commenced with a fit nearly thirty years ago leaving 
him with right hemiplegia. Recovered to a certain extent and 
able to work. Subject to fits since and delusions of persecu¬ 
tion, which caused his admission to Claybury asylum. Cause 
of death, ulcerative colitis. 

R. B., aged 47; occupation, porter; admitted to Claybury 
asylum on September 10, 1897. 

Notes from case-book. —Physical examination. Large scar on 
penis and a number of old scars on the right leg, inner Bide of 
left ankle, inner side of right thigh. General nutrition good. 
Pupils equal and react to light and accommodation. Knee-jerks 
increased on both sides. Fine tremors of hands, no tremor of 
face; co-ordination good. Urine, acid 1,025; no albumen; no 
sugar. Heart: Cardiac dulness increased. Heart sounds 
feeble. Pulse 68; small; regular. Lungs nil. Viscera nil. 
His sense of hearing is considerably impaired on both sides. 
Tactile sensation is said to be impaired in both legs. Right grasp 
is feebler than left. 

Mental condition. —Is able to give the following account of 
himself, which appears to be reliable. Was born and always 
lived in London. Went to work when 14 at a shop. Has lived 
a fast life with loose women and has drunk heavily. States that 
he has had fits for the last five years coming on once a month. 
He has no warning aura. He bites his tongue when he is in 
these fits. The first fit he had was thirty years ago, and this left 
him paralysed on the - right side, and since then he has used a 
crutch. He has delusions of persecution and thinks that the police 
are after him. He has hallucinations of hearing and vision. He 
thinks that the police are round his bed at the present time, that 
they are talking about him. He gets very depressed before the 
fits are coming on. 

Diagnosis. —Coarse syphilitic lesion.—H. W. L. 

No important change is noted until his death, but the following 
note was made on August 12. He is suffering from epileptic 
dementia, with frequent epileptic fits. His answers to questions 
are fairly clear, but his reasoning power is very slightly developed ; 



his mental reaction is somewhat slow. He has had syphilis. He 
is in fair health and condition.—R. J. 

September 20.—Pain in abdomen; temperature 103°. 

September 22.—Crepitations at bases of both lungs. Tem¬ 
perature 103'6°. Diarrhoea ;• motions mainly blood and slimy 

September 23.—This morning pulse weak, 140. Respirations 
37, laboured. At 5 p.m. he became unconscious, when seen 
was sweating profusely; breathing hurried; pulse frequent and 
of low tension. His right pupil was dilated and his right arm 
and leg were flexed and paralysed. There was no facial paralysis. 
He was only semi-conscious ; when shouted at was just able to 
answer questions. The unconscious condition deepened and 
death ensued. 

Post-mortem notes .—Post mortem. The salient features alone 
will be mentioned. Syphilitic scars on the body and on the 
penis as previously described. Skull, 6 to 7 mm. in thickness. 
No thickening of the dura or of the pia arachnoid. There was a 
good deal of congestion of the veins opening into the longitudinal 
sinus and those of the Sylvian fissure. Vessels—on the basilar 
artery there is an aneurism about the size of a large Barcelona 
nut, projecting to the left and making a small indentation on the 
pons. This swelling has several small yellow nodules in its walls. 
On cutting through it, it is seen to be filled with an organised, 
dense, fibrous substance, which grated on being cut, and con¬ 
tained a considerable amount of calcareous matter. The aneurism 
had been formed by a bulging out of the left side of the artery. 
The vessel, for two-thirds of its circumference, was unaffected, 
except by a thickening of the wall, so that the lumen of the 
vessel was uninterfered with. In fact, the aneurism may be said 
to have undergone a very satisfactory natural cure. The brain 
weighed 1,170 grms., and after hardening in formaline was ex¬ 
amined, and it was found that the whole second and third frontal 
convolutions of the right hemisphere have disappeared, and 
nothing is left but the pia arachnoid at the bottom of a cavity. 
The two frontal lobes are adherent in front along the mid-line. 
On cutting up horizontally the formaline-hardened brain it was 
observed that there was a patch of old softening, involving the 
anterior part of the gyrus fornicatus and base of the first frontal 
of the left hemisphere. At the level of the middle of the optic 
thalamus the softening of the left hemisphere was seen to 
extend into and have caused atrophy and sclerosis of the whole 
of the anterior portion of the internal capsule in front of the 
genu. At a lower level still, through the pulvinar of the thalamus. 


there was obvious atrophy and sclerosis of the anterior half of 
the internal capsule. There was no old or recent softening of 
the internal capsule of the right hemisphere. The vessels are 
generally thickened, especially the small ones. Microscopical 
examination of the vessels showed a condition of universal 
endarteritis; generally speaking, not nodular in character. 
Examination of the cord, after hardening in formaline, showed 
diminution of size of the lateral column on the right side and 
well-marked sclerosis in the crossed pyramidal tract; sclerosis 
slight in the left pyramidal tract. Ditto in the posterior columns. 
The other points noteworthy are :—Old pleurisy in the right side, 
commencing atheroma of the aorta, some chronic Bright’s disease, 
very acute ulcerative colitis, afifeotiog the whole of the large 

Case 42.— Endarteritis obliterans of the vessels of the circle of 
Willis. Slight cerebrospinal meningitis, almost total occlu¬ 
sion of the basilar artery. Severe headache and mental 
depression and hallucinations of vision. 

H. H. N., admitted into Claybury, April 1, 1896, for melan¬ 
cholia. A man aged 45, married twice, six children alive, two 
dead. Denies syphilis but has been in the way of getting it. 
No history of insanity in the family. Engine driver by occu¬ 

History from wife. —About a year ago had a very bad frontal 
headache whilst at work. He had to ask for relief, and went 
home exhausted, and could not wash or attend to himself as 
usual. He could not get any sleep. He became melancholy and 
began to worry himself about imaginary troubles in connection 
with his children. He also began to dread poverty and refused 
to speud money. His appetite failed and he would sit for half- 
an-hour without moving or saying anything. He became so 
gloomy that his wife bad to watch him. He was then taken to 
Highgate Infirmary, and from there was sent to Claybury, after 
remaining four days. 

November 5, 1896.—The man seems to have been a very 
sober, steady, and industrious workman, and his wife says he 
has been a model husband. He was never fond of company and 
always used to bring his money home. He has been married 
twice. His first wife (and child) died in childbirth. The eldest 
child by the present wife is 16. He was only married to first 
wife for ten months and a fortnight. One of his children by the 
present wife died in a fit at fourteen months. The patient is an 

122 : ■■■ ; '• AiKhUvm ; 

ra^lHgent. map •#$. jhik- ol 'is. good, fttjt >»e is 

extremely depressed aihI giooniy Ou admission eoiild only 
taJks '.fluid food aud that with ditticiilty,. but his appetite and 
general condition have much improved, He is a wtdl-wftdeman. 
.ate! .twad ter weigh-'*! m- a rule. His.visu&l hallucina¬ 

tions. im that the* ground looks like glass and ii» eb/si&arsd by small 
infieota of ohapgi«g colours. 'the faces of the *>thw patients 
moreover look swollen, especially cm the right side lit has 
nofcycOti this tor about kbreo avueks and ,hha tried io : &tiiv§ against 
it. Be is contented and resigned," Xfiero IS no \ytipipem about 
the face. The left pupil is larger than the, right, but very little. 
He is sold ip liftvo bad seixxuis*- but denies it. His pupils react 
to light: The {Keesitre blurred hut they »ce other , .vi^e normal. 

general pamlyfda:. . 

At the post ruprtetni basic syphilitic (?) meningitis? was fotind; 
with obliterative endarteritis to a greater or less degr^o of All. •tfe 
vesseta fornuag Usd circle of Willi*. The basilar esp&ciaily wgs 
affected, so that In one part its lumen was alnwst destroyed 
The Small vessels in themembrane yvfeip also markhiUy affected 

PHOTOWlt'ftQUIUL'a ». 

TrimsVWWft section of tin; vessels of the circle. »f \VJlUs. Observe .the 
basilar on the left h&bd side is almost bctluidl. SiS^oifwikti&U Si diameter*. 


The pia arachnoid of the spinal cord was to some extent 
thickened, but the vessels did not show any obliteration of their 
lumen. No doubt the severe headache he had suffered with, 
and probably the psychical phenomena were due to the menin¬ 
gitis and associated arteritis (vide photomicrograph). 

The arteries examined microscopically showed no tendency to 
atheroma. Still there is nothing specific about such an arteritis, 
and, in the absence of signs or history of that cause, syphilis 
is only problematical. The thickened pia arachnoid membranes 
at the base of the brain and covering the spinal cord examined 
microscopically showed a round-celled infiltration like the menin¬ 
gitis of the known syphilitic cases; so that the probability is the 
case was not one of arterio sclerosis, but syphilitic arteritis and 
meningitis. Probably this case was of a syphilitic nature, for I 
find it recorded in the post-mortem notes that there was a scar on 
the penis. 

Case 43.— Syphilitic endarteritis. Softening in the pons (diagnosis 
dementia paralytica). Secondary descending degeneration, asso¬ 
ciated with this there was degeneration of the fibres of Goll's 
column due to primary degeneration of the posterior spinal 
ganglion cells. 

A. J., female, aged 29 ; occupation, nil; admitted into Claybury 
on October*5, 1893. 


Family history. —Mother, three aunts, grandmother, and 
grandmother’s sister all insane (?). No phthisis, alcohol, con¬ 
sanguinity, nor syphilis. 

Previous history. —Subject to fits for the last ten years. No 
history of injury. 

Present attack. —Symptoms said to have been present for ten 

Condition on admission. —Poorly nourished. Pale and looking 
ill. Bruise on left side of body. Smooth paper scars on right 
shoulder and both legs. Tongue clean, moist, tremulous. Palate 
broad ; teeth fair ; appetite good. Heart normal; pulse 72; 
irregular, good volume. LuDgs normal. Eyes: pupils, right 
larger than left; right fixed; left reacts to light and to accom¬ 
modation, but very sluggishly for distance. Sight of right eye 
almost gone. Sight of left eye good. Ocular movements: left 
side normal; right external strabismus; no ptosis. Paresis of 
the muscles of right arm and leg; left side fair strength. Grasp 

'J24 ■viit'.UjyfcS: 

of lelc band good, 6iut very feehlo, drags ('.he right foot. Patellar 
reflexes exaggerated <m both sides, Articulation A; ottca-ftwcf; thick 
»«d slow. 

itupid, ironfuaed, and has 

She is heavy 

hut little idea pf time or p).o£&- Memory for recent add remote 
events? had. She is unable to give ber history, weeps wb«» any¬ 
one ;speaks to her .without any apparent cause, Reaction h? 
rjapstions very sluggish : $he Hprognaut (six months).- ' 

Di'iqni'Siis,—- Paralytic, dementia; 

.PHor‘*M(c»o(iB*j'H 8. 

8th cervical segment. Degeneration of QoII’b column and the eroRsed 
pyramidal .tracts, also of the direct UnetB. There is moreover a weil-trifo-ked 

ProtJfuStf. —She continued in the s&uie condition as on admis¬ 
sion until December 21, 1893, when she was eonlmed of a 
healthy female child; The child did not thrive auu \vha tenph^d 
by the parish.. -At the end of 1891- dovetopod opilbp.tifprnt 
Bei«m*ea, the* patifre of w hich are notdaspribed. During the year 
1895 the aofes : mmiA hp tneiital oi: WHiy.cha-ngs o«)y epiifeptt- 
fofm sei:<nr«H at intervals. At the end of 1895 I saw tins 
patient and suggested: tbai it wii* sypliiiiite brain disease. probably 
softening in ihb pen-*. She was put on iodide, but without any 


benefit. In fact, wheitTtsiiw her she was bedridden. Thex'p w» 
Contracture in both leg£ and right ariii Marked nysjtagtn«!s ;to 
tbe. .-lelty passing eve-ryth/tig under. her, unable to make- herself 
understood when questtoned, altliougb she attempted to do So,:- 
uildshe died *t few vhontba later.S. 

wortetn about fcw^ntyf^UT; ho.urailfteir 
death, Bpdy jK#ojrly nourished. Post-mortem rigidity- present 
throughout. There Ayere old tissue-paper .-scare pit left ;leg%ed a 
sore on each hip. Skull «yuiojet-rical and of fair thickness. The 
dura .{flatter tvas tbvekimd and 11u> .subdural *iflaoe contained an 
excess ot fluid The \pia~-&nU!h&04<l was thickened, opaque and 
stripped readily. The subafachuoid ftpauii con tamed an oxces? of 

PHW' iVlt ueoturu it. 

-4tb 'dowal (Agment. jP^euencdun in •"oltv a.udtbo kmmwh! 

pyramidal .tract.: ftiw alighti? in dh-eor, tft& If. will b? ftemd dixt tbero 
iti* «ejj marked trutngui&r am. of soU-rosis i.n.-tUo-of ouc 
.sidaaiid a slight diffuse • elt.mi.i •./ tbe htbyr ’ no dciulii this >? duo to tbe 
k-siou m the pou« oatwiftg dohCQudiflg dojxeufti'iitioij. 

fluid. There was syphilitic di*.&su of the vessels Jo the Sylvian 
fissure of both sides.. 'Atheroma- of bUKilar artery The train 
and cord Averu kept intact for furthest' examinatiath There was a 
patch of old softening which bad boconid sclerotic ifly.ibe right 
side of pods.•; Thus-bronchial glands were, pigmorded. Thdre \yas 
<ede®a and congestion *t the base of heitfv luu^BTb* heart, 
weighed ounces; the valves werehotth*!. with'-ihe'skb'e^lahu- 
of ;fehe : mitral, AyJfluxh. . *v*£ 

pale and fiirui and there was slight atlierbjrua of. the ecu Onariein 
There was atheroma of the aorta. The peritoneum arid omentum 

■. • . 

ooiitiiitied a very small amount of fa(., Tun liver weighed .4$. 
Ounces, was dark in colour,hbrou?and iffttkyy. were r»o 
stones iathe gall bladder and thereof viscid 
bile, dark in colour. The spleen weighed 51 mace siaiid- wau 
lar^ .ind edft- The. kidaoys weighed four ounces each and were \vere iioiamii arid the bladder 
vim contrue ted- and empty There was a ltuge cyst the size of a 

r»a>nH'auf)iio.<;.iiU‘U iO. 

S*!i-tuni of .ind lumbar; dfcg»;uemi.ioj! of both crossed fiyiuravJal tiiu&v, 
ihg-.-ncrutiou of (•VogeiiiHis tifWs of po-sUoiotiViHimijs., ft Will, bi 
that tlitt cojciili conimrssUrAI Kbi^s, tig? mWhiS.n oval ^tcfcfisigc and 

the poKtoio internal .triangle are intact Ti>, ,*• »n>, lm*-vor, endogenous 
■•.yilem *wv that the posterior eoiHmrt degyuerafinn coireiipbadij'W'itlj thal of 

pigeon’s egg i« the right ovary. Cause of death—syphilitic 
brain disciv; T K StAu*(i<4>L 

MiemtCiigi'Cnl udfes by dP- ;W,._ ilofch—faclerosis of ^pons, Up- 
geMratiyii of loug tracts. Endarteri^.' Uyphilitiea. Thiokfeiung 
of imminges of cortex IT ardethug'; fjtptV—.Mii'llor . Staining 
inetbods— $troebe. There is a general thickening 

of the j»a amahaoid over the cord and whole base of the brain, 


also over the meninges or the co.rtex. The vessels wera howhwis 
found obliterated, but there is a marked thickening of the ehdari 
terium us ft great many of the vessels seen in section, fn Sobye 
the endarteriiim is thicker than the remainder of the Wall of ihe 
vessel; bat nowhere did I find occlusion. The right crus -cerebri, 
is sinafjhr than the left*, so isvof the pons* The 
degeneration ■ of. the pyramidal tracts in the cord, however, is 
practically symmetrical. In the upper part of the pons at its 
juhCtion with the right crus cerebri if an area of sclerosis the size 
of a grain of wheat. . Both third nerves ale degenerated, but 


PnoToarttieoftAi'n U. 

Section of spina) cord at level ot ijrt «w;rA( sagnuuyl; shaping no ccMi-Se 
aegtmora.ti6a -in posttsriOr rolamn, -but-. ccftfcefi 

pyramidal tracts 

especially fbe right, though o. 

undestr<?yed. There is degeneration of the fillet on that side, 
obvious to the. naked eye in Weigeit preparations and of the pos¬ 
terior part. of iha. capsule. The cortex cerebri shows 

The cells, with the exception of the superficial 

pi a ariwhnokl 

layers are seen in "Weigert sections apparently nonnal, but 
Nisei’s method was not apphed. I cannot anywhere 


a difference of lire fillet-on two sides at fill comparable with 
that ahpye the lesidtt. There appears Hi be wiislirhJarbel'-ilegnoet- 
atioKi of'both tire p/rauiidn of the moduli eg but more mailed on 
liSmwise '-©T gonsb v^’itefcw' i4&KteBtoiH ^o^hy ,>pf 

Gull's column and of the funiculus gtaciUs. Burdach'$ ttueleus 
and eolarou are unaffected. Examination of the Jumbar posterlov 
spinal ganglia and roots- showed a most wtermirng condition 
which would entirely coincide and account for the atraphy of. 
the fibres uf uolam,i;i and subsequent sclerosis The 

VOtorosocTtpcHiAPU 12. 

Scctiorv dt*Dgitadittat> tit 'd$hy bun tar xpitiai ganglion 
degenerated celts Very di-epli M-vgoiDestiou 25, 

:hy»h.« -is- 

ganglion, out in eelloidliu dtid stained by Straebe raethcKV showed a 
number of large ©ells yrhiClr were tec46ureii red by the eaiJYantti 
and t>o nucleus was visible. A large hittnl»r of fibres, both 
pro-sitnal and distal to the ganglion were seen degenerated and 
atrophied, corresponding, no doufety to the degotiei'MM pelfe. 
Thie condition, is seen in the accompanying photomicrograph (12) 
or the whole ganglion under a low power showing, a large 
number of cells degenerated. The seel inn was stained by 
Bad method after eelioidin and all the degenerated ceils are 



stained blue instead of remaining unstained. Fatty degener¬ 
ated muscle gives this staining reaction. Consequently it is 
probably a form of fatty degeneration. The accompanying 
photomicrographs exhibit symmetrical degeneration of the long 
pyramidal tract systems (first cortical efferent neurons), and the 
posterior median (first cortical afferent neurons), vide pp. 124-127. 
Both system degenerations are probably due to trophic changes 
in the neurons, for neither of these symmetrical system degenera¬ 
tions can be accounted for by the unilateral lesion of the pons, 
nor by a meningo-myelitis. The degeneration so obvious in the 
antero lateral region of one side in the cervical and dorsal regions 
and not seen in the lumbo sacral is due to the unilateral pontine 

Case 44.— Cerebrospinal syphilitic meningitis. Peri-arteritis and 
enderteritis. Iritis three months before admission and three 
months prior to that acute mental symptoms set in with severe 
headache and vomiting. Pigmentation of skin. Diagnosed 
as Addison's disease. 

C. F., a married woman, aged 35, the wife of a soldier; 
admitted into Clay bury asylum on June 20, 1898. She came 
from the parish of St. George’s-in-the-East, under certificate as 

Facts indicating insanity. —She states that she sees snakes in 
her bed. She talks incoherently. She has suffered from frequent 
outbursts of mania. There was nothing noteworthy in the family 
history pointing to hereditary insanity or disease. 

Notes taken from case book. —She had been married seventeen 
years. There were two children, the youogest was aged 14. 
She had been of a cheerful, happy disposition until twelve 
months ago. She was temperate in her habits. As a child she 
had lived in India but she had always had good health, with the 
exception of an attack of enteric fever some time ago. Her 
husband states that last Easter her right eye became bad (iritis 
and keratitis). About December 24, 1897, acute mental 
symptoms set in. She was unable to sleep and she asked for a 
knife. About that time she complained of headaohe and vomited 
considerably. The vomiting lasted some months; she attended 
Guy's Hospital, but without benefit. 

Present condition. —Physical.—Height 5 ft. 1$ in., weight 
7st. 3 lbs. Dark hair. There are bruises on both arms and the 
legs ; there is a tissue paper scar the size of a florin, but somewhat 




irregular in outline, just below and inside the left knee. The 
tongue is clean and moist, the palate broad, and the teeth fair. 
Examination of the lungs and abdomen revealed no abnormal 
physical signs. The pulse is 84 regular, and the temperature is 
normal, and it remained normal or sub-normal throughout 
illness. There is a corneal opacity of the right eye. The left 
pupil is irregular (old iritis), and there is sluggish reaction to 
light. There is nystagmus to the left. Muscular strength is 
feeble, but there is no paralysis or tremor. The reflexes, super¬ 
ficial and deep, are brisk. Sensibility apparently was not tested. 
Mental condition.—She is very confused and cannot give a 
coherent account of herself. She makes contradictory state¬ 
ments. She is very restless and troublesome, and will not stay 
in bed. She says she has a snake in her inside. She has no 
knowledge of time or place. 

March 23, 1898.—I was asked to see her by Dr. Taylor, under 
whose care she was, as he thought it might be a case of Addison’s 
disease. The pigmentation was a diffuse brown coloration, 
particularly around the waist and over the left elbow, and I did 
not consider it characteristic of Addison’s disease, it was not 
around the nipples and axilla nor on mucous membranes; the 
scar on the knee, together with the corneal opacity and iritis, 
pointed almost conclusively to syphilis, although no history could 
be obtained from her husband. I recommended mercurial inunc¬ 
tion and iodide. She was treated for a week, and, as she did not 
improve much, she was put on suprarenal extract by Dr. Taylor. 

May 1, 1898.—She came under the care of Miss Dove, M.D., 
who made the following notes:—Has not improved much since 
last note. Seems weaker and complains a good deal of her head , 
but is bad mentally. Has not been sick for several days. Pig¬ 
mented spots seem more marked. 

May 16.—On the night of the 14th began to be much weaker, 
more restless, constant side movements of the head, delirium, 
with marked hallucinations of. sight and hearing, picking bed¬ 
clothes, &c. Nystagmus marked. She is now unconscious and 
somewhat drowsy. Takes nourishment well. Has not been sick 
since 14th. She is very weak. Has ptosis of left eye well 
marked, and slightly of right. 

May 19.—Gradually became weaker and died, 4.58 a.m. 

Post-mortem notes. —Post-mortem within twelve hours of 
death. External appearances:—State of nutrition fair. Old 
paper scar just below left knee. Good deal of pigmentation about 
the body. Skull normal thickness. Bight frontal lobe adherent 
to the dura. Pia arachnoid over the convexity, normal in thick- 


ness and somewhat dry and sticky. Weight of brain 1,220 grms. 
Convolutions flattened. Cortex firm, no excess of fluid. The 
base of the brain presents a characteristic appearance. The 
basilar artery and both vertebrals are much thickened, of a dirty 
white wash-leather appearance; likewise the middle cerebral 
arteries and the other vessels of the circle of Willis. The surface 
of the pons, medulla, and interpeduncular space is covered with a 
semi-solid, gelatinous layer, not unlike gelatine culture medium. 
This surrounds the cranial nerves, especially the optic and third 
nerves, but also all the cranial nerves arising from the pons and 
medulla. The brain was preserved intact in Muller’s fluid, also 
the spinal cord. The patient died of pneumonia, affecting the 
whole of the left lung, and commencing in the base of the right 
lung. There was atheroma of the aorta. All the other organs 
appeared normal to the naked eye.—F. W. M. 

Microscopical examination of the base of the brain, the brain, 
and the spinal cord showed a general cerebro-spinal meningitis, 
much more marked at the base of the brain than elsewhere, with 
general endarteritis and periarteritis. There are no coarse 
degenerations of the spinal cord or nerve roots. The spinal 
membranes are markedly thickened, and here and there, as in 
the pia arachnoid covering the medulla and base of the brain, 
there are irregular patches of coagulated serous exudation, and 
this substance is recognised by its deep staining with carmine. 
Extending along the neuroglia septa and around the vessels is 
this same coagulated material, forming curious irregular patches. 
It can also be seen in and around the nerve roots. It is probably 
caused by serous exudation into the cerebro-spinal fluid by the 
diseased vessels and the inflammatory process affecting the 
cerebro-spinal membranes. At the lower end of the cord the 
endarterium of the arteries is but little affected. Examination 
of the gummatous deposit at the base of the brain covering the 
pons, medulla, and interpeduncular space shows thickening of 
the pia arachnoid membrane by a round-celled granulation tissue. 
The neoplastic formation involves especially the vessels, forming 
here and there little nodules of gummatous tissue (miliary gum- 
mata), due to coalescence of several small vessels affected with 
marked periarteritis and endarteritis. The vessels are universally 
affected with endarteritis and periarteritis, though in varying 
degree. In some situations the arteries are little affected intern¬ 
ally, and a little further on there is nodular endarteritis, almost 
sufficient to occlude the lumen. All the cranial nerves, especially 
the third and optic, are affected to some extent, being surrounded 
at their seat of origin by the gummatous tissue, but it does not 



seem, generally speaking, to have affected the roots sufficiently 
to have produced any marked degeneration, when examined after 
staining by Weigert method. Apparently there are giant cells in 
the membrane. It seems to me that these giant cells are lymph 
coagula with granulation corpuscles imbedded in them. The 
appearance of the deeply-stained substance is exactly like that 
described as existing in the membranes and substance of the 
spinal cord. 

Comment. —The existence of iritis about a year would suggest 
that this woman was infected not so very long before the brain 
symptoms commenced to manifest themselves. 

Case 45. — Cerebrospinal syphilitic meningitis. Endarteritis, 
almost complete occlusion of the basilar artery. General 
affection of all the cerebral and spinal arteries great and 
small. Acute onset after heavy drinking. Death twenty- 
five days later. 

S. F., aged 34; occupation, fish-porter. Had served in the 
army in India. Admitted into Claybury asylum on July 8, 
1897. Died, July 20, 1897. Certified as hemiplegic dementia. 
Received no antisyphilitic treatment. 

History from mother of onset of illness.—Twenty-five days ago 
her son oame home complaining of a pain in the back, stiffness of 
the neck, and pain in the back of the head and neck. He was 
violently sick for two days and unable to leave his bed. Mother 
thought it was due to intemperance, for upon the day he was first 
incapacitated he had taken nineteen pots of beer. She had him 
removed to the Shoreditch Infirmary because he developed signs 
of delirium tremens, as she thought. He remained there a few 
days and was then transferred to Claybury. The following are 
the more important notes obtained from the case book :—He was 
certified as insane on account of delusions and hallucinations, 
incoherence, and dirty habits. 

Physical condition on admission. —Height, 5 ft. 5 ins. Weight, 
9 st. 4 lbs. Old syphilitic scars on neck, left leg, and thigh. 
He is in poor health. Suffering from right hemiplegia. He has 
difficulty in swallowing, and his water has to be drawn by 
catheter owing to stricture. He lies in bed helpless with a 
vacant expression. Takes no notice of what is happening around 
him, nor even what is done to him, as in passing the catheter he 
does not in the least show any sign of feeling. His nutrition is 
fair. There is nystagmus. 

Mental condition. —He is demented, dazed, and confused. 


Can give do account of himself, and takes a long time in respond¬ 
ing to any questions. He can give his name in an indifferent, 
heedless sort of way, therefore, although the notes do not state it, 
probably he was not aphasic. 

July 13.—There are no signs of improvement, in fact he 
seems more dazed than ever. There are no obvious physical 
signs beyond some dulness at right base. Bhonchi all over the 
chest. Heart apex, sixth space slightly displaced outwards. 
Continuous hiccoughing except during sleep. On July 17, coma 
gradually developed and pyrexia. Retraction of head and neck, 
and opisthotonos was observed prior to death. 

July 18.—Temperature, 104-2°. Sponged with relief, but 
temperature rose in the afternoon to 105°. Coma deepening. No 
squint. No increase in palsy. Meningitis. (The rise of temp¬ 
erature was due probably to the pneumonia.—F. W. M.). 

July 20.—Died from exhaustion of syphilitic meningitis and 

Post-mortem notes. —Post-mortem thirteen hours after death. 
Post-mortem rigidity well marked. Poorly nourished. No bed¬ 
sores. Scar on penis. Skull thin, normal, no disease of the ear. 
Brain congested, convolutions flattened, surface sticky. Ven¬ 
tricles dilated, contained clear fluid. Ependyma smooth. 
Venous congestion marked. Whole base of the brain, especially 
the inter-peduncular space, filled with a jelly-like semi-solid 
deposit. This involved also the membranes of the spinal cord 
down to the lower extremities. All the vessels at the base of the 
brain are white or wash-leather-looking, opaque, and thickened, 
and the basilar artery is almost obliterated, for a bristle cannot 
be passed along its lumen. Cultures were taken from this mem¬ 
brane in broth, gelatine, and agar, but nothing grew. Bight 
pleura, old firm adhesion. Bronchitis. Bronchial glands pig¬ 
mented, breaking down. Bight lung, hypostatic pneumonia. 
Left lung, well-marked lobular pneumonia with oedema; mainly 
lower lobe, but some patches in upper. Heart, aortic valve, re¬ 
cent vegetation. Muscular tissue, soft, friable. Spleen, soft, dark, 
becoming diffluent. Bight kidney, small abscess in cortex, in 
medullary region full of greenish offensive material. Left kidney, 
fatty, pale, greasy as was the right kidney. Bladder dilated. 
Mucosa nil. Cause of death, syphilitic meningitis and pneumonia. 

Microscopical examination of sections of the base of the brain 
and of the spinal cord at different levels, showed the pia arachnoid 
greatly thickened owing to a round-celled infiltration. This 
caused enormous thickening of the adventitia (periarteritis), and 
associated with it was endarteritis, in some places nodular in 



character, producing a half-moon appearance in transverse 
section; in others the inner coat was affected generally by the 
inflammatory process, causing almost complete occlusion. The 
small arteries are many of them completely blocked up by the 
inflammation of the inner coat; this is seen even in the lower 
end of the spinal cord. The roots of the cranial and spinal 
nerves are involved in this inflammatory process. There were, 
however, no coarse degenerations of the spinal cord or nerve 
roots. The vessels in the substance of the mesencephalon and 
spinal cord are all surrounded with leucocytes and gorged with 
blood, likewise those of the roots of the cranial and spinal nerves, 
and even the spinal ganglia show marked evidences of acute 
inflammation. Vide photo-micros 13 and 14. 

Case 46.— Case of general syphilitic nodular arteritis, followed 
by multiple softening. Diagnosis in case book, dementia post 
apoplectic. First indications, mental depression and stupor 
six years ago. Family history strongly supports diagnosis 
of syphilis. 

A. M., aged 51. Admitted May 10, 1895, to Claybury. 


Physical condition. —Heart, presystolio and systolic murmur. 
Feeble pulse, irregular in force and rhythm. Gait uncertain. 
Knee-jerks much exaggerated. Ankle clonus left foot. 

Mental. —Speech is slow. Patient is dull and heavy with a 
bad memory. Very depressed and weeps. States she feels at 
times as if she would like to die. Takes little notice of sur¬ 

On April 11, 1896, the following note was made: She is 
suffering from dementia. Her speech is somewhat suggestive of 
general paralysis, but it is not very tremulous. Her memory 
is greatly impaired. She does not know her age or her past 
history. She does not remember those she sees daily. She is 
well-nourished and stout, but drags her legs along on walking, 
and has to be helped everywhere. Knee-jerks brisk.—R. J. 

April 14, 1897.—She is suffering from senile dementia. She 
is exceedingly lachrymose. Tears begin to flow when one looks 
at her. She is not capable of conversing on the simplest ques¬ 
tions. She sits about and takes no interest in her surroundings. 
She is stout, plethoric, and paraplegic.—T. E. K. S. 

No note as to the existence or not of syphilis, but the follow¬ 
ing history was obtained by me from the husband. 

PaoTc^ictt<><>a.%p« la. 

•Civso 4ft.—Action- of lower end >*( lumbar spaiAl cord and posterior root 
l jwig^tinn of vessels ahowh ; pia n mo h t\of &j u fil traced with’ k J uefteyi*»i 

At the upper part i$ tv njttj&l! artery with the lumen greatly di Iftitiished by 
cud arteritis'. The walk b£ this vessel and the rnemhraires appear to l>e 
covered.’with’ mituitb patut^. These, uodot & lii&li po\v*n, r»rr 5 seen fcrt be round 
Mi\grmIcatiori AO diamsr^. 

V* lilel 



Antwrioarroot f.K'tti the dorsal **Kmu out longitudinally, slumiug 
of the MM of Iht?. -'iiVrvM by imn jailed UdiiliVAiou. $} the middle c*i vhe 
luwtJe feoffor is a vem intiltmted witlt l&ucogyto.. MaguidcaiidU TOO 



Married at 26. She was quite healthy up till six years ago. 
She has had seven confinements, but there is only one child 
living, a son who is 22 years of age and quite healthy. 

The first child died at birth. Then two miscarriages, then 
the boy who is alive, then two still-born, then one who died at 
birth. There is no history of insanity in the family. 

Abstract of notes from post-mortem book. —Post-mortem, 
general nodular arteritis cerebri, atheroma of aorta, third 
degree. Wasting of convolutions. Slight thickening of pia 
arachnoid, no adhesions, no granulation of ventricles. Multiple 
softening throughout the brain both in the cortex, the white 
matter, and basal ganglia. In the white matter the spots of 
softening ranged in size from a pin’s head to a hazel nut; one 
was found in the tip of the left occipital lobe as large as the 
latter. The immediate cause of death was tuberculosis and 
pneumonia. This case is very similar to the case recorded by 
Mr. Tredgold. 

Case 47.— Deaf and dumb patient. Delusional insanity, six years 
before admission to Claybury. Marked arteritis both middle 
cerebral arteries. Scar on penis. Insanity possibly due to 
arterial disease. Extraordinary small cerebellum and pons. 

F. P., male, aged 54, single, was addmitted into Claybury 
Asylum on December 11, 1894, under the following medical 

He was very exasperated and infuriated with his father when 
I entered the room, saying that he was annoying him (patient 
was deaf and dumb, so must have spoken by signs). He also 
said that he could hear voices speaking to him from the chimney, 
the bed, and the cupboard, that the people in the next room 
made noises like hammering and machinery. He could hear 
their voices abusing him, people call after him in the street and 
use filthy language. 

The father states that the patient was under the delusion that 
the house was a bad one, and that, he the father, had sexual 
intercourse with the other lodgers. Also that they annoy him 
and abuse him and make a hammering noise against the walls, 
and that he can hear their voices calling to him through the 
walls and down the chimneys. He wanders about the streets 
and accumulates rubbish, is miserly over it and considers it 
valuable. One of the lodgers says that he is very disgusting 
in his manner to her, makes beastly noises with his mouth, 
points at his person, and makes filthy suggestive signs to her 
on his fingers. 


The case book states that his bodily condition on admission 
was as follows:—His height is 5 ft. 4^ in. and his weight 
9 st. 7 lb. His tongne is normal, his palate high and arched, 
his teeth poor and his appetite fair. His heart, pulse, and lungs 
are all normal. His sight is stated to be fair, his pupils equal, 
and have a normal reaction. He is deaf and dumb. His knee- 
jerks are normal. 

His mental condition is stated in the case book to be as 
follows:—He is very deluded and believes that voices use all 
sorts of bad expressions to him. He admits all the delusions 
attributed to him and gets into a violently excited state when 
they are mentioned to him. 

On December 18, 1894, there is the following note made by 
Dr. Jones in the case book :—He is suffering from melancholia. 
He is a deaf mute, but makes signs that he is annoyed at night 
and that people hammer under his bed. That his ears shake. 
He wants to go away. He is impulsive and passionate, is well 
nourished and in good health and condition. 

Until March, 1897, the notes given contain nothing note¬ 
worthy, but on the 31st of that month there is another note by 
Dr. Jones, which states that the patient is suffering from 
melancholia. Gets very excited without reason. He thinks 
people are against him and steal his things. He is a deaf mute 
and can only talk in signs and by life imitation. He is very 
noisy at times and in good bodily condition. 

On May 6, 1897, he was discharged on trial, but was brought 
back on July 3 the same year because he had relapsed, and it is 
stated could not get on with a woman he lived with who passed 
as his wife. He remained in much the same condition until 
October 24, 1898, when he died. The cause of his death is 
stated to be exhaustion of renal and cardiac disease. 

The case book also states that he had been in Grove Hall 
Asylum before he oame to Glaybury and that the existing attack 
was of about six years’ duration when he was admitted here. 
His occupation was a shoe repairer. When his friends came to 
see his body, I found out from them that he had been deaf and 
dumb from birth. That he was a ladies’ bootmaker and that he 
had lived a very rackety life. His father had supplied him with 
as much money as he wanted. The following facts were obtained 
from the same person in answer to a letter which I wrote asking 
her further questions relating to the patient. He had been at a 
school for deaf-and-dumb people. He could read and write. He 
could not speak with his lips, but only with his fingers. He was 
not married and had not had any children. He was the only 



member of the family who was deaf and dumb. She could not 
say whether he was stone deaf or not, as he always complained 
of hearing noises, as hammering on the wall. He had not to her 
knowledge had any illness and had never been paralysed. The 
attendant in the ward in which he died said that he could not 
speak, but could make ejaculations with his lips. He thought 
that he was stone deaf, as he never took any notice of any noises 
that were made in the ward, although he had a delusion that he 
heard noises of people speaking to him. 

Post-mortem notes. —Post-mortem was made about twenty-nine 
hours after death. The body had been suspended in the cold 
chamber for about sixteen hours. State of nutrition, poor. Post¬ 
mortem rigidity passing off. There was a scar on the penis, but 
no scars elsewhere. No thickening of long bones of limbs. En¬ 
larged glands in left groin. Skull, average thickness about 4| mm. 
Bight tympanum not thickened, almost transparent, ossicles 
healthy. Dura mater adherent on right side. Deafness could 
not have been of peripheral origin. Pia arachnoid very slightly 
thickened over parietal regions on both sides. Over the top of 
the ascending parietal and round the ang. gyrus of the right 
hemisphere there are little haemorrhages. Also over the top of 
the ascending parietal and frontal lobes of the left hemisphere the 
pia arachnoid is congested. There is no abnormal appearance of 
the vessels of the circle of Willis. There is extensive nodnlar 
arteritis of both middle cerebrals, but the lumen is nowhere 
occluded. The brain weighs 1,130 grammes; right hemisphere, 
523 grammes ; left hemisphere, 518 grammes. The convolutions 
are somewhat wasted; the cortex was not atrophied and striation 
fairly distinct; the white matter was softer than usual; the 
ventricles were not granular nor dilated, and the fourth ventricle 
quite free from granulation; the cerebellum and pons weighed 90 
grammes; the cerebellum small and atrophied and weighed 70 
grammes; the pons weighed 20 grammes and was excessively 
small. Bibs fragile ; right and left pleura healthy ; bronchi not 
inflamed ; bronchial glands enlarged ; right lung had an oid scar 
at apex. Considerable hypertrophy about the apices ; congestion 
and oedema at bases; lungs crepitate float in water; frothy mucus 
in bronchi, weight 458 grammes ; left lung, old scar at apex, see 
above; weight, 610 grammes. Pericardium—universal adhesions 
to heart which are readily broken down. Heart—valves normal; 
healthy and competent. The heart is enlarged, the left side 
dilated, muscular substance brown, firm; hypertrophied on left 
side; left ventricle measures 16-20 mm.; right side of heart 
dilated, stopped in diastole; here and there white plaques on 


inner surface of both ventricles; considerable amount of 
atheroma (third degree); in some places atheromatous ulcers 
are seen; elasticity diminished; coronary arteries patent. Liver 
weighs 1,058 grammes; peritoneal surface shows a few opacities, 
otherwise normal; slight fatty change. Gall bladder contains 
no gall stones. Spleen weighs 46 grammes, pale. Bight kidney 
—capsule strips without adhesions; pelvis of kidney is con¬ 
siderably dilated, calices being distended, and contains a clear 
fluid; cortex thin and pale, in some places less than 1 mm. 
thick, general thickness, 4*7 mm.; medulla in some places dis¬ 
appeared ; a few small cysts; granular on surface; weight, 65 
grammes. Left kidney—same as right; weight, 65 grammes. 
Intestines show some amount of enteritis. Bladder distended, 
contains about a pint of clear urine ; muscular coat hypertrophied 
and shows on its mucous aspect interlacing bundles of muscular 
fibres; prostate considerably enlarged. Joints—no enlargement 
or ankylosis of joints of limbs noted. Testes small. Urethra 
offers considerable resistance to the passage of a bougie. Micro¬ 
scopical examination to be made of brain, kidneys, heart muscle. 
Middle ear on right side examined, normal. Cause of death— 
Uraemia of chronio Bright’s disease. Nodular atheroma of both 
middle cerebrals. 

Congenital deaf mute, imbecile. 

Microscopical examination of the arteries showed extensive 
nodular arteritis of both middle cerebral arteries. The lumen of 
the arteries was encroached upon by a dense fibrous-looking 
material, but no fatty change was observed. 

Notes by Dr. Mickle , Grove Hall Asylum. —He states that on 
admission he noted defective cranial development and also that 
the left pupil was the larger and acted somewhat defectively to 
light and to accommodation (this latter apparently not being the 
case with the right). The knee-jerks were on the small side 
then. He was deaf and dumb; replied in writing; could lip- 
read to some extent and his gesture language was sometimes 
very expressive. When under the influence of delusions this was 
apt to be of an angry, vehement character and threatening, as 
also were the simultaneously produced inarticulate cries. He 
was suspicious, at times imploring forgiveness, for what he could 
not tell. He had delusions as to being followed in the streets by 
crowds of people, who made faces at him, especially women. He 
had delusions of being poisoned and of ill-treatment. His chief 
complaints, however, were of being annoyed by people hammering 
on the walls, and the vibrations of this imaginary hammering 
and thumping seemed to be felt very keenly by him. A similar 



complaint was of his being here amongst noisy lunatics. Latterly 
his written replies were often irrelevant or incoherent as well as 
querulous, and he either could not or would not give much 
account of himself. He was often noisy at nights, but I have no 
notes of my own of the tenonr of his ideas at night. 

Remarks. —This case is of interest on account of the small size 
of the cerebellum and pons. 

Case 48.— Syphilitic gummatous meningitis affecting the first 
temporal convolution, nodular arteritis of basal vessels, epilepti¬ 
form fits, severe neuralgic pains in the left side of head, 
subsequently aural hallucinations. 


A. M.—A widowed woman, aged 50, was admitted into 
Claybury asylum on December 11, 1897, under the following 
medical certificate:— 

Her memory is bad; she is very talkative but her talk is 
quite unintelligible. She starts on a subject and breaks off in 
the middle and starts on another. She cannot tell where she 
came from or where she is now. She is depressed and cries 

Her attendant states that she is very noisy, restless and 
mutters to herself. She gets out of bed, pulls it to pieces and 
tries to wander about the ward. She sleeps but little and does 
not eat much. 

When admitted she had been suffering for six weeks and was 
in a poorly nourished condition. There were bruises on both 
arms and left buttock. Old scars on head, face, chest and back, 
and also on right shin. Her feet were much cyanosed. Her 
tongue was coated, teeth poor, appetite fair, and bowels con¬ 
stipated. Her heart was rapid and her pulse soft and irregular. 
She was blind and could only distinguish light from darkness. 
The lens of the right eye was dull and opaque, while the left 
pupil was very dilated. Her muscles were flabby and wasted 
and the reflexes were absent. There is no family history given in 
the case book. On December 17, 1897, she was certified by Dr. 
Jones to be suffering from epileptic dementia and to have some 
ecchymosis of both feet, probably due to varicose veins. She 
was noisy and restless and had to be kept in the padded room. 
She remained in the same condition until May 10, 1898, when 
she complained of having severe neuralgic pains on the left side of 
the head. She was clean and tidy, and although demented she 
gave no trouble. On October 4, 1898, there is a note by Dr. 


Ewart which states that she suffers from severe epileptic attacks, 
and after these she becomes dazed, that her memory is defective, 
and that she is almost totally blind. 

In November, 1898, she is again certified by Dr. Jones, who 
states that she is the subject of dementia and suffers from 
epileptic attacks which are not frequent but are severe, and also 
that she has aural hallucinations. 

On January 21, 1899, there is a note which states that she 
has been suffering from pneumonia for the last week, from which 
she died on this date. Her temperature at death was 104°. 

Post-mortem notes (abstract).— Autopsy twelve hours after 
death. Cause of death broncho-pneumonia and fatty heart, due 
to coronary atheroma. Marked atheroma of aorta, third degree. 
Spots of induration and thickening of capsule of the liver. 
Tissue paper scar on inner aspect of left thigh. Double optic 
atrophy. Nodular arteritis of the cerebral vessels. Thickening 
of the dura mater and adhesion and agglutination of the thick¬ 
ened membranes to the brain, in the left middle fossa, especially 
to the left of the sphenoidal fissure. A portion of the brain is 
adherent also in the anterior fossa. The patoh of thickening in 
the dura was about the size of a half-crown and was adherent 
to the middle of the first temporal convolution. 

Microscopical examination of this patch showed thickening and 
agglutination of all the membranes to the brain with an abundant 
round-celled infiltration, which extended in places along the ves¬ 
sels into the brain substance. Many of the small vessels existing 
in this inflammatory tissue were found to have thickened walls. 
The apex of the tempero-sphenoidal lobe is softened. There is 
opacity and thickening of the pia arachnoid of the hemisphere 
but no erosions occur on stripping. Weight of right hemisphere 
523 grins., weight of left 500 grms. The convolutions are 
generally wasted. Microscopical examination of other portions of 
the brain substance around the Sylvian fissure showed a con¬ 
siderable amount of inflammation around the vessels, and here 
and there dense accumulations of leucocytes. Examination of 
the backs of the eyes exhibited well marked disseminated chorio¬ 
retinitis as well as optic atrophy. I have subsequently found end¬ 
arteritis of the ciliary arteries and a curious pigmentation of the 
thickened walls of the choroidal and retinal vessels. 

Case 49.— Syphilitic encephalitis and atrophy simulating general 
paralysis in a worker in lead. 

W. D. C., aged 34. Admitted into Colney Hatch in 1897. 
Worker with lead. Has never had colic, but there is a blue 



line on the gums. Contracted syphilis at the age of nineteen. 
Attended the Lock Hospital. Seven years ago he became para¬ 
lysed in both legs, especially the right, for which he attended 
St. George’s Hospital and Welbeck Street Hospital. I saw him 
for the first time in September, 1897. His speech is somewhat 
impaired, for there is a little hesitancy and slowness. Tremor in 
the upper lip. He cannot say words like “ preliminary,” but his 
conversational powers are pretty good. He had a fit a little 
while ago. The tongue is protruded in the middle line and there 
is no tremor. Pupils are equal and react to light and to accom¬ 
modation. There is a marked spastic gait; the knee-jerks are 
exaggerated and there is ankle clonus on both sides. He 
responds to the calls of nature and has control over the sphinc¬ 
ters. Wrist tap contractions can be obtained on both sides and 
there is a fairly good grasp in both hands. 

July 13, 1898.—Three fits running one after the other, 
became unconscious for some time, then he fell into a dazed 
condition for many days. His physical condition has not 
changed much since the last note. His memory, however, is 
decidedly more defective and he shows signs of dementia. He 
keeps repeating the statement that there is a lot of arsenic in 
bronze and white lead, and that the colours had got into him. 
There is still a slight blue line on the gums and an old scar of a 
gumma on the right leg. 

August 10.—He does not know the year, kept repeating that 
the colours have got into him ; had a fit ten days ago, losing con¬ 

Unilateral right-sided convulsions, with deviation of the 
head and eyes to the right. His speech is hesitant, but neither 
syllabic nor tremulous. The pupils are equal and react to light 
and to accommodation. There is marked exaggeration of the 
knee-jerks, triceps and wrist tap contraction can be easily 
obtained. No jaw clonus. Marked ankle clonus on both sides. 
There is weakness in both arms and legs. 

The patient died in March. 

Post-mortem notes. —Brain—dura not adherent; pia arachnoid 
markedly thickened and opaque over the following situations: 
over the superior and external surfaces of the hemispheres and 
along the meesial surface on the anterior two-thirds in the upper 
part. The portions of the hemisphere in which the thickenings 
are not observable are: the occipital lobe, the whole of the 
temporal lobe except the tip, the orbital surfaces of the frontal 
lobe and the convolutions adjacent to the corpus callosum. The 
thickening corresponds thus pretty closely with the area of dis- 


tribution of the veins which open into the longitudinal sinus. 
Especially the frontal and central convolutions are atrophied; 
the right weighs 555 grammes; left 545 grammes; pons and 
cerebellum weigh 160 grammes; the ventricles are granular, the 
fourth especially so; the lateral ventricles are greatly dilated; 
the cord appears very small in transverse section, and to the 
naked eye seems degenerated in the posterior and lateral 

Microscopical examination .—The cord, after hardening in 
formal Muller solution, was cut and stained by the Marchi-Pal 
method, at about the level of the 6th dorsal segment; degenera¬ 
tion with secondary atrophic sclerosis was found in the crossed 
pyramidal, direct pyramidal, descending tracts, and in the follow¬ 
ing ascending tracts: the posterior median and the ventral and 
dorsal cerebellar tracts. A very little above this segment the 
degeneration was limited to the ascending tracts, a very little 
below it was limited to the descending tracts mentioned, and then 
several long systems could be followed to their respective termi¬ 
nations above and below. This explains the paralysis he 
suffered from seven years before admission, which was no doubt 
due to a very localised meningo-myelitis. It also explains the 
spastic gait that he subsequently suffered from. This meningo- 
myelitis did not occur till eight years after infection, and was not 
an early case. Examination of the brain by Nissl method for 
the cells, and Marchi-Pal method for the tangential fibres. 

The appearances presented were not like those of an ordinary 
general paralytic brain section by either method. There was a 
chronic inflammatory meningo-encephalitis, but the cells all were 
arranged in definite layers, their processes could be followed 
to the second and third branches. They stained fairly, and a 
great many of the cells showed normal Nissl granules. There 
were great numbers of leucocytes in the peri-vascular lymphatics 
and in the brain tissue. The walls of the blood-vessels were 
thickened. The tangential fibres, although diminished in number, 
were nowhere absent, although the pia arachnoid was thickened 
and the seat of chronic inflammation. 

This case was one, then, of true meningo-encephalitis, with 
secondary changes in the neurons, as' distinct from primary de¬ 
cay of the neurons with secondary and associated inflammation. 

Remarks .—The clinical symptoms were not like those of 
general paralysis; he had no pupil phenomena. It may be that 
his continuous statement that “ the colours had got into him ” 
was not devoid of foundation. The lead combined with syphilis 
explains well the conditions found in his brain. 



Case 60.— Melancholia. Progressive dementia and paralysis. 

Nodular syphilitic arteritis universal and of old standing. 

M. D., admitted into Claybury on December 19, 1893. Died 
February 20, 1897. Age on admission, 35 ; occupation, none. 

The facts indicating insanity, for which she was admitted, 
were as follows: She is controlled by delusions of a desponding 
nature. Hears imaginary persons accusing her of being very 
wicked and declaring that she will be burned to death; also 
fancies she hears her husband and other absent persons talking 
to her. Her memory is very defective; she says she has been 
here five or six weeks whereas Bhe really came yesterday. She 
has no knowledge of time or place. 

Physical condition. —Tongue very furred, palate normal, teeth 
poor, sight fair. Eyes—pupils equal and react normally to 
light and to accommodation. Walk—gait normal, knee-jerks 

Mental condition. —Patient’s reaction is slow; she is rambling 
and somewhat incoherent; her memory is fair and she has no 
obvious delusions. 

Abstract of notes from case book. —There are no noteworthy 
facts mentioned until January 1, 1895, when the following note 
was made. She is suffering from dementia with general 
paralysis. She is dull and stupid and cannot give her name. 
She is very shaky and her speech is difficult to make out, as she 
is so tremulous. She is indifferent to her surroundings and is in 
fair health and condition. 

September 20, 1895.—Some weeks ago she upset a can of hot 
tea over her arms, which burned her. Mentally she is dull and 
feeble and is not very steady on her feet. 

July 16, 1896.—She is now in the infirmary, is very feeble 
and lachrymose; paresis more marked ; she is wet and dirty. 

January 18, 1897.—Patient is confined to bed; has advanced 
phthisis at both apices ; there is marked rigidity and contraction, 
and, as a result, is developing bed sores, though she is washed 
with the greatest care. 

February 20, 1897.—Patient gradually became worse and 
died at 11.50 a.m. this day. 

Post-mortem notes. —Post-mortem forty-six hours after death. 
State of nutrition emaciated. Post-mortem rigidity passing off. 
External marks—herpes labialis; tatoo marks on right arm; 
bed sores over both trochanters and over sacrum, marked oedema 
of feet. Skull much thickened, pale, dense; dura mater thick¬ 
ened ; subdural space contained an excess of fluid; pia arachnoid 


thickened, opaque, strips readily; sub-arachnoid space contained 
an excess of fluid. Vessels—nodular syphilitic arteritis of the 
basilar, vertebrals, carotids, the circle of Willis and basal vessels 
generally. Brain wasted and contained an excess of fluid, pale ; 
convolutions much wasted, simple, small and flattened, sulci 
wide; cortex very soft, small in amount, watery; white matter 
soft and watery; ventricles dilated, left more than right; 
ependyma granular; corpus striatum soft and watery; optic 
thalamus soft and watery; cerebellum soft, superficial veins 
enlarged; pons and medulla soft and watery. 

Bight and left pleura—old adhesions over apex. Bight lung 
—upper lobe made up of tubercular consolidations, surround¬ 
ing cavities containing greenish-yellow fluid; lower lobe con¬ 
tained a few tubercular nodules. Left lung—upper lobe similar 
to right one but not so chronic, few tubercular nodules in lower. 
Heart weighs 7 ozs., normal; aortic, small recent vegetation, 
size of small hemp seed between two posterior valves ; muscular 
tissue small in amount, dark, pigmented and fibrous. Liver 28 
ozs., pale and soft, a few scattered tubercular nodules. Spleen 
3£ ozs. Soft, congested kidneys; right 4 ozs., left ozs. pale, 
capsules slightly adherent, cortex wasted. Bladder contracted 
and empty. Ovaries and uterus appear normal. 

Case 51.— Multiple cerebral tumours, certified as epileptic mania. 
Subsequently character of fit noted as Jacksonian in type . 
Trephined skull, no tumour found, but temporary relief of 
symptoms. Autopsy : Tumours undergoing caseation found 
in various parts of the cerebrum, and one in the cere¬ 
bellum. Microscopical examination showed the tumours to 
have some characters resembling gummata, and others 
resembling tubercle. Existence of a few tubercle bacilli in 

M. A. B., a married woman, aged 29, was admitted into Clay- 
bury Asylum on January 21,1896. The following was the medical 
certificate under which she was admitted :— 

At the time I examined her she was in a state of acute mania, 
and placed in the padded room. She was talking rapidly and 
incoherently. She had a blanket folded up and held in her 
arms, declaring it to be her child, and that it had just gone to 
sleep. She also declared that she was then at home in her own 




Her mother stated that she had been forgetful for some months 
past, that she haa had a great number of epileptic fits. She had 
been violent, destructive, and restless, and has had no sleep for a 
week and takes no food. At one time she declares that she (her 
mother) was a monkey, at another that she is a baby, and she 
wishes she was dead. She drinks. 

She has been ill for two weeks before admission. She has not 
been under treatment anywhere before. She had a brother, died 
in Darenth Asylum of paralysis. She has had three children, who 
are all dead. The first died at fourteen days. Then there was a 
miscarriage. The next lived about a year, and the third died 
within a month. Patient had her first fit about the middle of 

1895, and her second attack of about twenty fits in January, 

1896. She drank heavily, chiefly rum, for about three months 
prior to admission. Her temperament was as a rule cheerful. 
When admitted into Claybury her bodily condition was as 

She had bruises and a syphilitic eruption on limbs and body 
and old sores on buttocks and back. Her tongue was clean, moist, 
and tremulous. Her palate broad and her teeth fair. Her 
appetite was bad and her bowels were regular. Her pupils were 
equal, and reacted both to light and to accommodation. Her 
heart and lungs were normal. Her reflexes are absent, and her 
muscular gait and walk are good. She was certified as suffering 
from epileptic mania by Dr. Jones in January, 1896, and again iu 
December, 1896. In the latter certificate she was stated to have 
hallucinations of both sight and hearing. She sees the place on 
fire at night, and hears people calling to her. She has had 
several fits, is fairly nourished, but in feeble health. 

On March 24, 1897, she had a fit, which is described by Dr. 
Stansfield in the case-book as follows:—The fit commences with 
twitching of the angle of mouth on the right side, then in sequence; 
slight winking of right eye and rubs nose with left index finger. 
Bight arm is extended, and the eyes turn to the right; the 
head turns to the right. Twitching of facial muscles of right 
side. Bight arm is flexed and pressed to the side, followed 
by clonic spasms. Bight leg extended; foot arched. During 
the fit the right conjunctiva is insensible, the left sensible 
(normal). The fit lasts about two minutes. As soon as the 
motor explosion has ceased she is stupid, but appears to under¬ 
stand slightly what is said to her; she looks about, frowning. 
The breathing is heavy, laboured, and snoring. When not having 
fits there is considerable hebetude and marked aphasia. She 
cannot name anything shown to her, but having been told the 


name of the article she applies it to everything else she is asked 
to name. She has a greatly impaired memory both for recent 
and remote events. At times, and these very frequent, she com¬ 
plains of pain in her head at the vertex. She vomits slightly in 
the early morning, sometimes before food and sometimes after 
food. There is no paresis, except perhaps slight in the facial 
muscles on the right side, and there is no part of the scalp 
specially sensitive. Her eyes have been examined several times 
by different people, but no optic neuritis can be made out. On 
August 13, 1897, it was noticed that there was now well-marked 
optic neuritis, more on the left than on the right side. It was 
thought that she was suffering from a tumour on the brain, and 
on August 31 she was operated on. The skull was opened over 
the lower end of the ascending frontal, the inferior frontal, and 
the ascending parietal convolutions. There was slight bulging of 
the dura into the opening thus made, and it was noticed that 
there was some slight thickening of the dura, and the pia arach¬ 
noid was so markedly opaque and slightly gelatinous in appear¬ 
ance that the possibility of general paralysis was suggested. No 
tumour was made out, and the wound was closed up. The patient 
bore the chloroform well, and when she woke up she was decidedly 
brighter and more intelligent than before the operation. She re¬ 
mained brighter until the end of September, and the optic neuritis 
was rapidly passing off. In the beginning of October she was not 
so well again, and she was operated on again, but again no sign of 
a tumour was found. She did not stand the anaesthetic so well 
this time, and had a number of fits about a month later. After 
this she gradually sank, and died on December 17, 1897. 

Post-mortem notes. —Post-mortem about fourteen hours after 
death. State of nutrition wasted. Post-mortem rigidity well 
marked. Skull: the space, where the bone had been removed, was 
filled by scar tissue, which was adherent to the subjacent brain and 
meninges. The sub-dural space contained no excess of fluid and 
the pia arachnoid was not thickened. There was no atheroma 
of the vessels and they appeared quite healthy. In the left 
occipital lobe and occupying nearly the whole of it was a tumour 
which was broken down in the centre and caseous at the peri¬ 
phery. Almost the entire left cerebellar lobe was occupied by a 
similar growth. The two were not adherent, nor was there any 
noticeable degree of meningitis over the situations of these 
tumours. Again, immediately under and in the cortex in the 
situations indicated in the diagrams (i.e., the inferior frontal con¬ 
volution posterior end and the lenticular nucleus of the opposite 
side) were growths also containing rounded caseous nodules. 



There were no granulations of the ventricles. There was old 
pleurisy of the right pleura. There was a small gumma in the 
upper lobe of the left lung and both lungs were congested and 
oedematous. The heart weighed 214 grins.; the mitral valve was 
slightly atheromatous and the muscular tissue was soft and 
flabby ; there was no atheroma of the aorta. The liver weighed 
1,109 grms.; there is peri-hepatitis and the liver was hobnailed 
and in a state of extreme fibrosis. The spleen weighed 430grms., 
was enlarged, and contained a small caseous mass the size of 
a hemp seed and was difluent generally. The kidneys weighed 
164 grms. each; there was hypostatic congestion and fatty 
degeneration. In the stomach there was post-mortem degenera¬ 
tion. The contents had escaped into the small omental sac, but 
there was no sign of peritonitis. The stomach contents were 
dark in colour.—H. W. Lewis. 


After hardening in formol the tumours were cut into, and 
revealed irregular nodular patches of caseation, in places coalesc¬ 
ing to form irregular tracts, while elsewhere the coalescing areas 
formed little islands and islets. In between these caseating areas 
are tracts and strands of greyish-red tissue, in some places firm, 
in others softer. Microscopically the caseous areas are seen to 
consist of a firm amorphous detritus, the only vestiges of formed 
structure being obliterated and tbick-walled vessels. The inter¬ 
vening greyish and greyish-red substance consists of a granula¬ 
tion tissue containing immense numbers of small, round cells, 
staining deeply with logwood, also congested vessels. As a rule, 
however, the walls of these vessels presented no marked endar¬ 
teritis. At the boundary of the caseous masses are great numbers 
of giant-cells. The irregularity of the caseous areas would favour 
gummatous deposit, so also would the history of the patient. 
Miscarriages, dead children, and likewise the peri-hepatitis. 
Microscopical examination of numerous sections stained with 
Ziehl’s fluid revealed no tubercle bacilli. Consequently, in spite 
of the giant-cells, which, however, have been described in 
syphilomata, all the evidence goes to prove that the growths 
were of syphilitic origin. After careful searching, however, I 
found a few tubercle bacilli in the giant-cells, therefore I must 
change my opinion and come to the conclusion that these 
tumours were tubercular, perhaps, however, associated with 


Case 52.— Syphilitic encephalitis (probable). Diabetes due to 
insterstitial pancreatitis with parenchymatous atrophy and 
degeneration. Almost total destruction of the organ. Stellar 
cicatrix, probably remains of old gumma , on under surface of 
liver. Scar tissue in patches on lungs. 

Clinical notes by Dr. Eobinson, to whom I am much indebted 
for calling my attention to this interesting case; also I wish to 
acknowledge my obligations to Dr. Church for his courtesy in 
allowing the notes taken at St. Bartholomew’s to be published. 

M. J. P., admitted October 14, 1889, aged 45, married, no 
children; no occupation. 

Previous history. — Patient has always suffered from bad 
health and seems to have become worse since the loss of her 
sister three years ago. She has attended several hospitals, the 
last being St. Bartholomew’s, where they told her she had heart 
disease, dropsy and diabetes. Whilst being treated there, she 
became depressed, would not take her food, so from there she 
went to Shoreditch Infirmary and then to Colney Hatch. She 
has been fond of stimulants, chiefly whisky, and when under their 
influence had delusions that she was “ Queen of England.” 

Copy of hospital notes. —She was admitted into St. Bartho¬ 
lomew’s hospital August 2, 1898, and discharged September 23, 
1898. She was under the care of Dr. Church. 

Clinical abstract of notes. —Six months previous to admission 
increasing feebleness. For one week legs swollen. Irregular 
heart; systolic murmur at apex. Glycosuria; sugar grs. xx. 
—ji.; average quantity of urine 5 pints; sugar cannot be fer¬ 
mented by yeast. Gives Phenyl-glucosozone crystals. Is dextro¬ 
rotatory, acting quite like dextrose. 

Clinical notes. —Well until six months ago; general wasting 
and becoming feeble; two weeks’ sickness; one week legs swollen 
and took to bed; jaundice ten years ago. Mother died of heart 

On admission she was in a dying state; extreme pallor; 
conjunctivas distinct, icteric tinge; tongue furred. Chest—Per¬ 
cussion good to bases; some moist rales ; heart sounds extremely 
irregular; much sacral oedema. Pulse irregular, not to be 
counted; no murmur detected. Heart sounds on average 160 to 
minute. Abdomen—nothing abnormal discovered. Legs blue'; 
some hard brawny oedema of legs. Urine—specific gravity 
10*22; sugar grs. 25£ to ji.; a trace of albumen. Patient too 
ill to be thoroughly examined. 



August 5.— Patient seems a little querulous; heart still 
irregular; rate still averages 160. 

August 6.—Heart better, 132. Urine, passing 5 pints daily ; 
specific gravity 1024. Sugar grs. 25} to ji. 

August 8.—Sugar grs. xx.—ji.; a trace of albumen; colour 
of lips and face improved ; general icteric tinge. Heart more 
regular, 96. Now the heart is acting more regularly, there is 
heard a soft systolic murmur at apex. Complains of sickness; 
oedema of hands continues. 

August 12.—Mentally the same, wanders a little at times; 
quantity of urine less; sugar, grs. xxx.—ji.; pulse slower, more 

August 23.—Sugar grs. xx.—ji., quaotity Oiiss.: will not take 
glutin-bread. Pulse intermittent 78. Heart sounds clear ; liver 
not felt; general condition better. 

August 29.—Patient declares she would rather die than take 
a diabetic diet, so she has been put on ordinary diet. 

September 10.—Patient seems to be no worse for her bread 
and butter ; sugar has increased; urine 3 pints. Heart irregular; 
systolic murmur present. 

September 15. — Acetone odour in breath; temperature 
throughout subnormal. Diet restricted but not knocked off. 

Upon admission into Colney Hatch she was a case of melan¬ 
cholia with suicidal tendencies, with no marked delusions; she is 
a fairly nourished woman, although feeble, and had upon ad¬ 
mission oBdema of feet and legs. Examination of lungs—Lungs 
are fairly healthy with exception of few rales at bases. Heart 
no preecordial bulging and no thrill; auscultation reveals a very 
loud systolic murmur at apex of heart which can be heard at apex 
of left scapula; heart sounds very irregular; she has a peculiar 
dryness of skin and is very anaemic. Tongue beefy and deeply 
furrowed; has a ravenous appetite and complains a great deal of 
thirst and passes large quantities of urine. Since admission she 
has been kept in bed owing to the oedema of her legs and shortness 
of breath; heart sounds very irregular; pulse low; tension 
irregular, at times scarcely perceptible; is taking slop diet and 
a mixture containing digitalis and senega every four hours, 
with good effect, the heart becoming more regular, so that 
after a few days she was allowed to get up and sit with other 

October 21, 1898.—Her urine was collected for twenty-four 
hours which amounted to 210 ozs., specific gravity 1035; a 
sample of this was taken and examined with a copper sulphate 
and potash solution, showing large quantities of sugar. Roberts' 


fermentation test was tried to show quantity per oz., whioh 
amounted to 27 grs. The urine in this way was collected for a 
week and each time showed same quantity of sugar although 
quantity of urine diminished, the average quantity being about 
150 ozs. in twenty-four hours. During this time no treatment of 
any kind was carried out. 

October 30, 1898.—Her sugar and potatoes were stopped but 
she became very discontented, and after about a fortnight of full 
restricted diet she would not persevere with it, so it was discon¬ 
tinued ; during that time the amount of sugar dropped from 
grs. xxx.—ji. to grs. viii.—ji., but when ordinary diet was taken 
again it went up to the usual grs. xxx.—ji.; she took cocaine, 
but it had such a bad effect upon her heart that it was discon¬ 

November 25,1898.—Patient is now in bed again with general 
anasarca of body and bronchitis; breathing greatly impeded; 
faoe cyanosed; pulse scarcely perceptible; she is taking slop 
diet and a mixture containing strychnia and digitalis; no 
marked result; anasarca being more extensive and her condition 
very critical. 

December 3, 1898.—She has commenced to improve; her 
medicine being changed to tartrate of potash, spirit of juniper 
and decoction of broom c digitalis every four hours; her heart 
is more regular; pulse stronger and quieter; breathing easier and 
anasarca diminishing; takes her food better; in this way she 
continued to improve, anasarca having disappeared, and was 
quite able to get out of bed until December 14, 1898. She had a 
seizure which affected the whole of left side of body and same 
side of face. (The following events happened.) The facial muscles 
on left side of face commenced to twitoh, then the head, includ¬ 
ing the eyes, were rapidly turned to left side; then the left arm 
is raised and clonic spasms of left arm, leg and face. These events 
following very quickly with total loss of consciousness, but she 
very quickly came out of them. There is a weakness of left arm 
but no paralysis; during that day she had four similar seizures 
and ten during the night, being in a very exhausted state. 

December 16,1898.—It was noticed for the first time that she 
had paralysis of left arm and leg and when the seizures ceased, 
which was upon January 14, 1899, after having in all 250 
seizures, the condition of her limbs was as follows: total 
paralysis of left arm, motion and sensation, with a weakness of 
left leg, but quite able to move it about. During this time she 
had become very emaciated and her mental condition was bad, 
being very demented and incoherent; she remained in this help- 



less and emaciated state until February 1, 1899, when she had 
another seizure and never regained consciousness, and died at 
10.10 a.m. 

Post-mortem notes .—Autopsy twenty-four hours after death, 
weather cold. Body emaciated ; dropsy in legs and left arm ; no 
scars; diffuse pigmentation on abdomen and inside of thighs; 
rigor mortis passing off. Cranium.—Skull: from the inner table 
in front are numerous projecting spicules and excrescences, but 
the dura mater is not adherent; a large amount of cerebro-spinal 
fluid. Brain 41£ ounces; very marked thickening of pia 
arachnoid, especially over paracentral lobules on both sides; 
non-adherent; ventricles not granular; dilated; no softening ; 
naked eye sclerosis, or growth in hemispheres. Pons.—Lefo 
pyramidal system smaller than right; over floor of fourth ventricle 
above calamus on right side, different appearance to left; smaller; 
greyish red; flocculus on either side, somewhat yellow; vessels 
presented no naked eye change. Thorax.—Pericardium, little 
fluid. Heart 9£ ounces; ventricles contracted; mitral valve 
much thickened; only admits middle finger; recent vegetation 
on auricular surface of valve; one vegetation the size of a pea 
attached by a stalk; aortic valves thickened; competent when 
aorta was filled with water; no hypertrophy of ventricle or 
dilatation; aorta atheromatous, first degree, most marked at 
coeliac axis. Lungs not adherent to pleura; right 14£ ounces, 
left 13 ounces. The whole of the visceral pleura of the base of 
the right lung is white and thickened, but lung everywhere 
crepitates and floats in water. On the left lung there is an old 
white cicatrix between and adhering the anterior surfaces of the 
upper and middle lobe. Liver 41 ounces ; tough and fibrous and 
dark-stained ; numerous white thickenings of capsule, which ex¬ 
tend into organ; large stellar cicatrix on under surface of left 
lobe. Gall bladder contained normal bile; not dilated. Bight 
kidney 3£ ounces, left 3$ ounces; capsule adherent; no scars; 
no infarcts. Spleen—Small, normal; no infarctions; no thickening 
of capsule. Pancreas.—At first we thought the symptoms could 
be accounted for by the condition of the medulla, and not much 
care was exercised in getting out this organ, but it was noticed 
that in order to detach it from the duodenum the gut had to be 
cut, thus preventing us afterwards finding the entrance of the 
duct. The organ was obviously extremely small, and there was 
a cyst in the head of it connected with what was apparently the 
dilated and obstructed duct. There was hardly any of the gland 
left. All that could be seen to the naked eye consisted of vessels 
and duots surrounded with fibrous tissue. A more definite 


statement tan be made as to the nature oi these large vessels (?); 
dstets dU^t^J whew a microscopical eKaaiioatidir has beeix made. 
Obviously the gland is extremely-, ^opWe'd'*’-’. Portions were 
taken m fm-mol, and in spirit and also is glycerine. The ovaries 
end iiterus preaeiited eathiiig abaofm&l, opr did the trvueous 
meihbrwine <d luc stomach, Fottj.ona of in spirit and in 
forniol. The;- *dyiis>n«e extract of the organ bad no digestive 
attion upon ftV'en hoiled sfareb or atbiiufien When artificial diges¬ 
tion w$8 tried, .a feir dropa.(10 m.) being added to 3 per cent, 
solution of sodium carfxorutfce.. 


| Vp&l.ohaM, showing adyftnrftd derbmi* and dilated ducts. Ou 

t!<U -faTCi* » Jiiiiail portion of glai><j giliisiapati, bht all tiie calls arc either' 

coagulatuin nWd'wis A yfeition (if fchfos lobule 
Sa'^Wniw^^liok^ntdrogntpb IS.- MaguifiestHui tiO d»»inatgrK. 

of tbv gaMOirea^ liver, 
scar opliver and scar ou pleura were cut after the tissues had 
been libihodded in uelioidia and stained with logwood and eoaio. 
Sections of the brain were cut after eathoddiag in,paraffin. Ail 
the sections showed an indaiiimattSfy 1 process of some standing 
with secondary parenchymatous- atrophy and formation of scar 
tissue. Ip the liver it had the j^wi^ticaiial, pro¬ 

ducing imiuieratitiftl hepatitis, fix the sears of the liver and the 
pleura it had given origin to patches of dense cicatricial tissue, 
but there was no eVideoce of caseation. In the darted cerebri it 
had also caused patches of soar tissue. 06 doubt accounting for 

154 : avbivks 

ibe fits*. The partcroaa' jwuj -been. probably the aoat of. the earliest 
and jaofet it^a>uj'e£»tt|fun *; df&b the glandular ^tmciure of; 
tlit. organ had been almost- entirely destroyed, only fibrous tissue, 
ducts itud vetmtda being ipftv ,$Ke process wan most. .advanced V 
the bead of the organ, no skniho bhiokmg the duct, causing cystic 
dilation and dilatation of the tributaries of. the main duet, 
The organ consists of dense fibred* tissues, dilated duets, and 
decaying parenchyma • the whole, gland, or what ie left of it 
being infiltrated with round cells (letrcoeyigH). 

FfU) l r»^Mjeueaiuu‘n 1C. 

A snmll portRiii cif the .tfUnU fUihutenci.', ■showing acute irifi«mrns.tioif 
which guitt: obscure* the proper of the paroucliynis. MhgUiftofttioD 800; 

The lobules of the gland that are still left are. rthdei ft high' 
power, seen th of heilfit;tyhph;;bh^^- 

necrosis, and other cells whiob do not show so ad vanced a prunes^ 
of degenerafioo..: ’TV *ells that are apparently dead are stained 
UD.ilormly a rliffuKc reddish purple. The nucleus is tint visible.- 

vm' I : ‘ . i. :‘.L" W: v.::‘:V' ■:*.. -i’ •’ J V • ' , v « 

Tfas ^car^to^.) : )Wg ^how ite 

presented by the gecutwas-,, 

limailcs opon thi$ The pointy pf: interest are.;, (1 ).thg 

association of diabetes with desirhction of the pancreas; (3} 
IV occurrence of fite asebbia'ted with a chronic encephalitis and 
fcaVatioii of scar tissue on the cortex corcht-i; (3) syphilis 
probably the cause for the following reasons. Patient ie & 
married woman with no children. The appearance of the 


cranium, the scar on the liver, the scar on the pleura, and the 
chronic inflammatory process in many of the viscera all point to 
a constitutional poison. The naked-eye and microscopical 
character of the lesions accord with what we know syphilis pro¬ 
duces. Lastly, the diffuse pigmentation on the abdomen and 
inside of thighs is strongly corroborative of this view. 

Case 53 .—*Case diagnosed as epilepsy and dementia. Remained 
in Hanwell Asylum seven years. Autopsy : Old gummata of 

R. A. M., admitted October 10, 1891, aged 24. Married, 
three children, two dead, died young. First attack, duration 
unknown, said to be seven days; is epileptic and suicidal, but 
not dangerous; is fourteenth of a family of fourteen. Previous 
disposition cheerful, amiable, industrious. Habits temperate ; 
father intemperate. 

Diagnosis on admission .—“ Dementia and epilepsy." 

History .—Could not be obtained. Mother stated that her 
daughter was quite well and ought not to be detained. 

On admission .—Was demented, memory bad, simple, childish, 
&c. Bodily, was in weak health ; system normal. 

Course of the disease .—Has been noted as having frequent 
epileptic seizures and fits of violence and destructiveness. 
Habits dirty. Suffered from recurring attacks of maniacal 
excitement, lasting some weeks. Frequently injured herself. 
About seven months ago became gradually paralysed. 

Condition in May, 1898.—Thin, pale, anaemic, bedridden. 
Very obstinate, spiteful and abusive, using what power she 
had to resist examination. Complete paralysis of left arm 
and left leg. Kuee-jerks normal on both sides. No rigidity 
present. Pupils normal. Sensation could not be tried except 
pain, which was present. There was present such marked signs 
of acquired syphilis, such as typical scars on both legs and 
about the knees, also thickened tibioe, &o., she was put on 
anti-syphilitic remedies and the paralysed limbs were regularly 
massaged. Face was never paralysed. Under this treatment 
some improvement occurred. Partial movement returned to 
the leg at the hip and knee joints, and the fingers could be 
moved. This improvement did not advance. Spasticity came 
on, exaggerated reflexes and ankle clonus, and some rigidity of 
both arm and leg. 

Died from phthisis pulmonalis, November 28, 1898. 

* Editorial note: I saw this case, and pointed out that it was a case of 
organic brain disease due to syphilis. 



Post-mortem, examination was held twenty-four hours after. 
Head.—(1) Calvarium, hard, dense, diploe practically absent; 
increased in thickness; (2) dura mater—no change to naked eye ; 
not adherent abnormally to calvarium ; (3) special condition— 
heptomeninges appeared normal. No surface lesion. On pal¬ 
pation a hard area was felt at the tip of the occipital lobe on 
the left side, and a similar area at the upper part of the Bolandic 
area on the right side. The consistency of the brain as a whole 
was much increased. On section into these hard areas growths 
were found. The Bolandic one appeared to be a gummatous 
growth, beginning on the mesial surface of the brain about one 
inch below the vertex, and growing fast in an upward and then 
in a downward and outward direction below the cortical grey 
matter of the Bolandic area, taking with it a sheath of pia 
mater ; it then turned somewhat inwards. Antero - posteriorly 
it extended from the anterior part of the ascending frontal 
convolution to a little behind the ascending parietal con¬ 
volution, cutting it a little over the upper £ of the Bolandic 
area. It was surrounded by a zone of softening, pink in colour. 
Structurally it was dense and hard, with a point of softening 
in the centre of the older part. It was light yellow in colour. 
The occipital growth on the other side was much less, but had 
the same characters. Arteries to naked eye diseased in places. 
The pons and medulla were very hard, particularly the olive 
on each side. The pineal gland was hypertrophied. The brain 
weighed 43 ozs. The membranes of the cord were very much 
thickened and very vascular, and there was present a large 
increase in cerebro-spinal fluid. Cord removed for further ex¬ 
amination. Brain preserved. Section cut of growth which 
revealed round cells, small and large, in strands of fibrous tissue 
and areas of degeneration. Lungs.—Acute phthisis present. 

I am indebted to Dr. Lord for tbe above notes of this case. 

Case 54.— Syphilitic brain disease, twenty-three years after infec¬ 
tion. Deafness, aural hallucinations, optic neuritis, vomiting, 
headache, fits, dementia. Improved markedly under anti¬ 
syphilitic treatment. 

G. W., male, aged 43; bricklayer. Had syphilis twenty-three 
years ago, and was treated for it at St. Bartholomew’s. In the 
beginning of October, 1898, he began to feel very sleepy, and had 
a severe headache. He never felt any sickness and gradually 
went deaf. He was taken to Bethnal Green Infirmary, where he 
was said to have abscess of the brain. He was there for a fort- 


night, and then was removed to the London Hospital, where he 
became insane and was removed to Claybury Asylum. He had 
aural hallucinations. His pupils were unequal, the right being 
widely dilated, while the left was normal. The right only acted 
to light and to accommodation. His speech is very drawling, 
and there is tremor of the lips, and more marked tremor of the 
hands. He was certified by Dr. Jones to be suffering from 
dementia, as having no idea of time or place, to be wet and dirty 
in his habits, and to have scars on his head and on the lower 
part of the right shin. On October 31, he is said to have paresis 
on the right side of his face, and well marked optic neuritis in 
the right eye, with some blurring of the nasal side of the left 
disc. He has not been sick, nor has he complained of headache 
since admission. On November 22 he had two seizures, when 
the left side of his face, left arm, and left leg were convulsed, 
and his head deviated to the right. He was comatose during 
and after the fits, and his temperature on the left side was higher 
than the right. He was put on anti-syphilitic treatment, getting 
30 grs. of potassium iodide three times a day, and a drachm of 
ung. hydrarg. rubbed in twice daily. He continued to improve 
under this treatment, and got less deaf and more intelligent, and 
was discharged recovered on February 23, 1899. On February 
25 he came to Charing Cross Hospital. He has complete deafness 
in the right ear and partial in the left. The pupils are inactive to 
light, but react to accommodation. There is no tremor in the 
tongue or lips, and no speech affection. His knee-jerks are 
exaggerated. There is optic neuritis in the right eye, but this 
is clearing up. He still continues to improve under anti¬ 
syphilitic treatment. 

Case 55.— Syphilitic arteritis in a woman, resulting in right hemi¬ 
plegia, followed later on by general paralysis. Post-mortem : 
Endarteritis syphilitica, sclerosis of the right pyramidal 
system, characteristic lesions of general paralysis. 

E. H., aged 37, a married woman; has been in Claybury 
several years; according to her own account, since a fit four years 
ago, when she lost the use of her right side. She is unable to 
give any clear account of herself. She was born and lived in 
Chelsea, is married, and has had four ohildren, all of whom are 
dead. Her husband has deserted her. One aunt, her father’s 
sister, she stated, died in an asylum. Her father was probably 
alcoholic, but her account was not clear. The patient’s appear¬ 
ance and speech are very characteristic. She walks with a 



shambling gait, has a fixed, unmeaning stare, her lips are 
tremulous, her speech thick, blurred, and scanning. She begins 
the sentence with abnormal distinctness, the voice raised and 
getting hopelessly confused in her articulation after the first few 
words, missing syllables and leaving sentences unfinished. The 
tongue is tremulous, and protruded unevenly. She holds the 
right hand with the left, and the right side of the face shows 
rather less marked folds than the left. Her mental condition is 
one of mild exaltation. She has no very definite ideas of grandeur, 
but she has an exaggerated way of speaking when trying to tell 
anything. She is emotional and readily moved to tears or smiles, 
but quickly passing from the one to the other. Her powers of 
concentration are practically nil. She appears to understand 
questious put to her, but cannot give a connected answer; memory 
appears also to be defective, and this may partially account for 
the inability to do so. She can read fairly well, but tires soon. 
Her temper appears to be good, and she is industrious so far as 
her infirmity allows. Her habits are not dirty, and she has no 
definite delusions so far as can be ascertained. The attendant 
does not know about her sleep. She appears to have no fits now. 
There is some loss of power on the right side of the face. The 
• right palpebral fissure is a shade lower than the left; the right 
cheek shows less tone. There is a very slight degree of right 
ptosis. Both pupils are dilated, and do not react to light or to 
accommodation. The pupils are equal but irregular. There is 
paralysis of the superior rectus, shown by inability to move the 
eyeball upwards, all attempts at this resulting only in the un¬ 
covering of a wide band of sclerotic between the iris and the 
upper eyelid. The right arm shows diminished power; no 
movements cure absent, but the grasp is noticeably weaker than 
that of the left, and it is with the left hand that the patient helps 
herself. The arm is flabbier as a whole than the right, and the 
nails of this hand more uneven. There is no noticeable differ¬ 
ence made out in the legs, but, in addition to the paresis present, 
inco-ordination is also well marked Patient is unable to pick up 
fine objects without great effort, to bring the tips of her fingers 
together, or to touch the tip of her nose. Her handwriting shows 
this remarkably well, and is somewhat like her speech. Wat ching 
her, one sees her making strenuous efforts to make a clear stroke, 
but the pen waves feebly over the paper, and after a few attempts 
she has to give up. She steadies the right hand with the left, 
but makes no attempt to write with the latter. The knee-jerks 
are extremely active. A slight degree of ankle clonus is obtained. 
The superficial reflex is also increased. 


Sensation. —Tactile; no impairment detected. Sensible to pain. 
Temperature and taste not tried. Hearing not impaired. Vision 
appears good, as patient can read fairly small type. Ophthalmo¬ 
scopic appearance of the fundi practically normal. There is no 
abnormality of digestive, respiratory, or circulatory systems 
detected. Amenorrhoea of several years’ standing. 

Diagnosis. —The patient, I take it, is in the third stage of 
general paralysis. The hemiplegia may have been the result of 
a cerebral lesion, probably vascular in origin, which was coincident 
with or possibly anterior to the onset of the more serious malady. 
Fits, with temporary or permanent paralysis, occur fairly fre¬ 
quently in the early Btages of general paralysis. The speech and 
the inco-ordination are later symptoms, and not, I take it, in any 
way connected with the earlier hemiplegia. 

Patient died three months after this history was taken. At 
the autopsy the brain showed the characteristic lesions of general 
paralysis, viz.:—Atrophy of the convolutions, pia arachnoid 
thickening and adhesions ; dilated and granular ventricles. The 
vessels at the base of the brain appeared normal to the naked 
eye, but careful examination of the opto-striate arteries exhibited 
well-marked obliterating endarteritis. The cord and medulla 
showed sclerosis of the right pyramidal system well marked, 
some slight Bclerosis only being found on the left side. 

Case 56.— General paralysis and syphilitic endarteritis; occlusion 
of basilar artery. 

M. B., aged 35, admitted to Claybury, September 20, 1895; 
occupation puella publica. 

On admission she is stated to be suffering with mania of general 
paralysis. Her speech is tremulous; she has grandiose delusions, 
she is very noisy, dancing and singing, and continually talking of 
diamonds and dresses. There is marked tremor in the muscles of 
the tongue and face; knee-jerks exaggerated. There is no note 
as to the pupils. Scars on the forehead, temple, and symmetrical 
scars on legs. A year later it was noticed that there was a 
marked motor impairment, but of what nature is not stated, but 
there is a note to the effect that she is likely to fall about, and 
she has a bruise over left eye through slipping down. Six months 
later the notes state that she is confined to her bed and that she 
is suffering from seizures. She died three months after. Duration 
of illness altogether was 1 year and 9 months. Notes from Case 

Post-mortem. —The brain weighed 1,187 grams, very wasted, 

1H0 ^ClttVES 


'j^a-ai%ch 0 Ojd;'tiyc^MiCf} v opaque and adboreirt, ^eufcriolee'dilated, 
ependyrna wry granular^ great excess of cerebro-spiaal fluid. The 
bagilar artery was tUrao&t occluded, a email poiunn was? out til 
sectiba®. arid these ^bowgd extreme. typical eddatteri^a 
pbotomiorogyapfi). Section of spinal cord Rbbwed well marked 
scleiyai'a in both «i owed pyramidal traots. Seat-iona pf cortex 
cerebri exhibited the iVutoal tojKroscoptiWbeharafttora of general 
paralysis. Absence of tangeutMt fibre*. atrophy of pyramids! 
•ofctb* great increase of apidet ©ails {vid* photomicrograph 18 u 

V;.., >/,' ^ ?>;; ’ .'V'-'- ;••. V 

tnvnsvem ngst-jon of Iwailar ftfl»]py ^]i«;lr^‘Jag 6i&rtt'ptis arid 

oiiuiMon.'' ‘^Digriinofttion- 40 Siai^e^sr.- • 

0^'^j^^^^,pi0iV(^^l^pr&J^9itktlenieHii^- in n tmrri&l 

Oifitnictid-jtjplulis t> iht itnng. in 
1882. Uhtui'ir Vf utittfaiM. tUiiUrin ■'!->/.'/ mismrrUvjq. . A'" 
%$tpr>; of vi'ilqi,-,!/ or inurifflPi foMiihj. 

F. S. €.. ivd.npif.tKl'' to. Coiney. Hatch, September 11 1898. 
Married, iert&nfc, it- P'aC-kiBiey.'^flioq,iHomejion, N.hl. Mot 

first, attack. Age on attack, 28,-present awe, 2b. Coh.ev 
Hatch .'fybhV.0eb>W' UH$7. ..$•> April 4, of 

existing attach, tunm days. Subject to epilepsy. No history ni 

insanity oc epilepsy to family. ‘,. 

VcrUfir.;>U \--.--'She is 3 deject to epileptic fits, she is sullen, 

is very depressed and tfiolaniiliplic at- times, She doee not know 


what she is doing. Sometimes when spoken to will gaze vacantly 
and will not speak. 

On admission. —Had slight bruises on arms, chest, and but¬ 
tocks, also old scars on right leg and foot. 

Previous history. —September 22, 1898.—Husband states that 
they have been married eleven years. The first two children 
were stillborn; third, a miscarriage (at five to six months); fourth 
ohild living, four years of age and healthy; fifth died, aged eleven 
months (chest trouble). Husband in army, 1880 to 1887. Con¬ 
tracted syphilis in 1882. Had sore on penis, eye troubles, rash, 
etc. Is now in impaired health, being an inmate of Homerton 
Infirmary, suffering from cardiac trouble. Age 38 years. 

October 26, 1898.—A few days ago had a succession of 
epileptic fits, also had another yesterday. Been very “lost” 
since admission, confused, understands nothing. Bestless at 
night, sleeps a little after a draught. Dirty in habits, strips 
herself, quite incoherent, but rarely talks. 

November 2.—Last two days patient brighter, takes food well, 
able to sit up. 

November 14.—Very helpless, cannot stand alone. Several 
fits since last note. Never speaks. 

December 14.—In a state of stupor, not confined to bed. 
When asked to walk, put out her tongue, etc., refuses absolutely. 
Has been seen to walk all right when she thinks she is not under 
observation. Knee-jerks excessive. No fit for three weeks. 

February 22, 1899.—Removed to the Infirmary. Had a 
succession of fits, nine in number, last night. Marks like bed¬ 
sores coming where no pressure is, i.e., on arm and thigh. 
Difficulty in swallowing. Is becoming very feeble. 

March 1.—Patient died this morning. —George A. Fleming. 

Post-mortem examination revealed the characteristic lesion of 
general paralysis. 

Case 58.— Congenital syphilis. Left hemiplegia from infancy; 
paresis and diminished sensation in both legs. Knee-jerks 
exaggerated , patellar clonus and triceps contraction left side. 
Diminished reaction to faradic current in both legs, especially 
left , and also in left arm. 

E. H., aged 34, came to Charing Cross Hospital, sent by my 
friend, Dr. Burney. Her elder sister accompanied her. She 
complains of pain in the limbs; she is very deaf, especially on 
the left side. She has typical Hutchinson’s teeth. Her sister 
has also notched peg-top shaped central incisors and old keratitis. 
The sister, a married woman, gives the following history. Mother 



had three premature births, then two children born dead, then 
one which lived sixteen months. She came next, and the patient, 
E. H., was born a year later. The married sister also informed 
me that she had had but one child, which was a delicate infant; 
it had snuffles and died at the age of six weeks. I have been 
unable to find out if her husband had Buffered with syphilis; it 
would be extremely interesting to know if the germinal plasm 
can be modified by the syphilitio poison; for it is conceivable 
in the Weismann doctrine of the continuity of the germinal 
plasm that the effect of the poison may not be limited to the first 
generation, especially if it be remembered that the ova are all 
present in the ovaries at birth, lying dormant till puberty, when 
the sexual and reproductive instinct with which they are 
inseparably associated arouses their vital activities. The patient 
E. H. has been paralysed in the left side since early infancy. It 
was discovered only by her not being able to walk or use the 
hand. When quite an infant she had a rash on the skin and the 
eyebrows came out. Later in life it was noticed she was deaf in 
the left ear. The left arm and leg are wasted, and the bones 
smaller. She has no contracture. There is a triceps contraction 
and marked patellar clonus, but no ankle clonus. There is 
marked diminution of sensibility in the lower limbs. Last 
December she was affected with pains in the legs and left arm; 
there is diminution of reaction to faradic excitation in the lower 
limbs and in the left arm and impaired sensation in the lower 
limbs. She feels perfectly in the upper limbs. There is no 
loss of control of sphincters. Fundi normal; hypermetropic. 
The wasting in the upper limb is not confined to any par¬ 
ticular group of muscles. The hemiplegic condition was pro- > 
bably of syphilitic origin, though it may have been a case of 
infantile paralysis. She is troubled with irregular menstrua¬ 
tion, and the recent symptoms were thought by Dr. B. to be 
hysterical, as the condition varies a good deal at different times. 
The family history is the specially interesting feature in this case, 
as showing the effects of acquired syphilis upon the offspring, 
and also the possibility of transmission to the third generation. 
The mother came to see me and said that she had never ailed in 
any way, and I could find no evidence of syphilis on the body. 

Case 59 .—Congenital syphilis. Father and mother both died of 
organic brain disease. This case illustrates the effects of in¬ 
fection in parents and children. 

M. G., aged 36 now ; admitted into Caterham asylum in 1879 
for imbecility, where she has remained up to the present time. 


I obtained the following history from the aunt:—Father con¬ 
tracted syphilis, married, infected wife. She does not know 
whether there were miscarriages or premature births, &c. Eldest 
child, M. G., was able at one time to talk and walk. She was 
sent to the aunt when she was 15, but she became so much worse 
mentally and physically that she had to send her away. Before 
she did so, she took her to the Lock Hospital and the girl was 
seen by Mr. Alfred Cooper and five other doctors, who all said 
that it was a hopeless case. She had lost the roof of her mouth 
and was becoming deaf and blind. She was apparently quite 
healthy till 5 years old, but about that time she began to have 
ozsena. The father died, aged 36, of brain disease, oaused by 
the syphilis, in 1868. The mother was sent to Prestwich 
Asylum in 1875 and died eighteen months later, aged 36, of 
organic brain disease. 1 A son, who was imbecile, was sent to an 
asylum and is still there. There are two younger children, 
women, who are of low type intelligence and moral instinct. 

The girl M. G. is deaf and dumb and partially blind. There 
are opacities on both cornese, the result of old keratitis. The 
bridge of the nose is saddle-shaped, the skin earthy, and there 
are linear cicatrisations around the angles of the mouth. Upper 
jaw : both right central and lateral incisors gone and left central 
erosions of enamel; lateral carious. The lower incisor teeth are 
all very small, peg-shaped and with marked linear erosions of the 
enamel. Pupils irregular, unequal and do not react to light. 
She is quite demented; only makes a humming noise. The 
body is well-nourished. She walks with a spastic gait and feet 
inverted. Knee-jerks + +. No ankle clonus obtained. Scars of 
old gummata on both legs. She iB regular. * Catamenia normal. 
Wet and dirty in habits. June, 1899.—F. W. M. 

Case 60.— Syphilis ; man aged 23. Neglected treatment; six years 
later, dull frontal headache, slight hemiparesis of face and 
tongue, followed later by typical ataxy, with marked sensory 

1 was asked to see this case, as being possibly one of syringo¬ 
myelia. The notes stated that there was a doubtful syphilitic 
'history. The man, however, told me he had had a chancre; he 
was treated for six weeks at St. Peter’s Hospital; that he went 
no more, the sore having gone, he believed he was cured. Seven 
months later he had an ulcer of the tongue, which got well with 

1 This was confirmed by a letter from the Medical Superintendent to me. 



mercury and iodide of potassium. He is nearly bald and he has 
enlarged cervical glands and shotty indurated inguinal glaDds; 
but because he had no signs of a skin eruption it was presumed 
that the history of syphilis was doubtful. Ataxy was diagnosed 
by me as he had Argyle-Robertson pupils, absent knee-jerks, 
marked inco-ordination, ataxic gait, Romberg’s symptom and 
bladder trouble. 


I wish especially to acknowledge my indebtedness to the 
following three admirable monographs, to which I would 
refer readers for further information upon this special 

Oppenheim. Die Syphilitischen Erkrankungen des Gehims. NothnageVs 

Lang. Pathologie u. Therapie der Syphilis. 

Foubnier. Les affections parasyphilitiques, Paris, 1894. 


Allbutt, Clifford. St. George's Hospital Report, No. 3. 

Alexander. Deutsche Medicinishe Wochenschrift, No. 41, 1881. 

Barlow. Pathological Soc. Trans., vol. jxviii. 

Beaudouin. Contribution a V etude de syphilis grave pri*coce. Thdse, 
Paris, 1889. 

Braus. Him-syphilis , Berlin, 1873. 

Bristowe. Pathological Soc. Trans., 1859, vol. x. 

Broadbent. “Syphilitic Affections of the Nervous System,” Lancet, vol. i., 

Charcot. Ltcons Cliniques. 

Chabrier and Klippel. “Etudes anatomo-pathologiques et cliniques des 
arterites c^r^brales syphilitiques.” Revue de Mi*d., Sept., 1894. 

Crocker. “Diseases of the Skin.” 

Dittrich. Prager Vierteljahrschrift, 1849, p. 42. 

Erb. Archiv fur Klinische Medicin, July, 1879. 

Fournier. La Syphilis du cerveau, Paris, 1879 ; La Syphilis liered. tardive, 
Paris, 1886. 

Gilbert and Lion. “De la syphilis m6d. pr^coce,” Archiv. gen. de vied., 
1889, 2. 

Gowers. “Diseases of the Nervous System.” 

Von Graefe. Archiv, 1860, vols. i., vii., viii., xii. 

Grob, Leon, and Lancereaux. Des affections nerve-uses syphilitiques, Paris, 

Heubner. Ueber die Himerkrankung der Syphilitischen, Archiv der HeiU 
kunde, 1870, vol. xi.; Die Luctischc Erkrankung der Him-arterien , 1874. 

Hirschfeld, Birsch. Archiv der Heilk., 1875, p. 170. 

Hitzig-Oppenheim. Ibid. 

Hjellmann. “ Om Hjsirnsyfilis des frekvens kronologi, etiologi, ocli 
prognos/* Akad. af. Handl ., Helsingfors, 1892. 


- *>. %phiii'ti^i6 far d*rm. n. SjjjjphV, X&Jl 

maim- ' 

>A*£JUa£. Arokl$. #t dzmL ri Styph,, .1874;. (\U<x A)t{t<iU d& Ifhwtttiiwn#i 
i* 79. 

^fK'XLtv #?,-& <m;? Foreitpi Ucd.^Chir. Hcvku>i t*~0, 1S74■; &l*o “Oenomi 
-- • 0if tbe• In^ue.; v / ; V ; -/ : .- X- 

MpfipH': ‘‘ Kttnjtif and PAtu/plcgle bt4 ; Am*. JJrd M vql xU 

^*CriftfN r . Btrltri Kllru Wwtiaiis^ lpfiy. ' V ' V-.'' 

No>w&; ’. Biitfidge^ KmntntU der Sypjiil. Erk .. 

0tvr^U3;>iO!H, NordiVcl. MedianUh). An.kic: t vfj. \, 
livVKK.- “La Syphilis 'crhvbrttie rv* M/rongienoo/' Amah eh Tfierup^ 1847. 
ftiOtuaiA' • &{i2$tte‘y$e-y : . , 184$.'/••.> -^r-^Jr j- ,'r-v‘V 

Hctmpp. . /jjrcjfciw. /. P&jckiafrw f Vo), xvi ; also /.Hr Syphiuti^L'-u B’tfmnir 
bUiUfm tUs -n^n!^i(s&M) %St\$s\kulvM t 'itif&i ;;v v •'" ; ' V-V^ :.'• : 

ToCMtite, Guj.e^mLAV pf'.yr*-* $fr# M 1882. 

TorBfeTrtf GjLLEft r*E i.^, 451) Ht DEtvO. •* Syphilis maligno invceoe/*' 

7 : •,'■> ; ; ‘ . ' '• V- 

UlirwoPF (x Z\i\ di^gnOst. Bedcutnog der Hcrlociori^b^n PupUlofsd*«.rt\v‘ 
Birf^uv hi in ffi&fuwwfoifi* 1880* s. o5; (cW d/.- te* dry S ur h,h-. 
xfas-;£irJ3^|^^A \i#?it*ii%un*J*'n x L^ipsd£., 

1847.■ Voi. xv;; i?eseput$telfi % : d’8(>9, voJL ih-y l 't?cb*-r 

di? Nat nr ,iVr Mjphil ...Affect ,, Bx?rV»ft,- iKdtH 

Wilks.' V'&P thy : ^'pii7)|6^-4^dCtidne-qf !»hfc iiateYtwl orf^uaV’ $<*?/> Ildfyitel 
deport*, 1883 )tS$fc 

Wt’$AT tfef‘ fcr&tn aiui spir$*l cord/ 1 f/trfnan 
CUnio.u Lr.cbir V', Syd S».#c, 

ZASdflico. ft# u&fy Paris, 1$>2. ; 

PiKiTOilICBOaiUPH 18. 

svction ot‘ brain of *»5, r.’iiov/Hig .overgrowth of gjia colls,, abduce c»f 

tfiwgoi^tml ftjyres.. Stained l<v W’eigek : > cftrinioo tiiothod. 

Part II. 


The dictum of Krafft-Ebing that general paralysis is 
a product of civilisation and syphilisation is finding pretty 
general acceptance abroad; but it is only recognised by 
some authorities 1 in this country. 

The chain of circumstantial evidence which associates 
syphilis with general paralysis is gradually becoming 
strengthened, the more the disease is studied. But what 
part does syphilis play in the production of the morbid 
process ? and what is the pathology of the morbid process 
underlying this terrible disease ? Some authorities would 
regard a history of syphilis occurring in a patient suffering 
with general paralysis as a mere coincidence; others would 
regard it as a more or less unimportant factor; others 
would see in it a most important connection ; whilst others 
would go so far as to say, no syphilis, no general paralysis. 
I shall leave my readers to form their own conclusion after 
studying all the evidence, although I shall sum up myself 
strongly in favour of the very important role syphilis plays 
in relation to general paralysis. 

If we regard general paralysis as a process of premature 
decay of the nervous system affecting the structures latest and 
most highly developed, it is not reasonable to suppose that 
a poison so prevalent, so potent and so persistent as syphilis 
can play no part in the production of this disease, possess¬ 
ing, as it does, such a powerful devitalising influence on 
all the tissues of the body, but more particularly on those 
which are subjected to injury, stress, or which inherit a 
locus minoris resistentice. 

I do not, however, consider the dictum “ no syphilis, no 

1 “ Syphilis ” does not even occur in the index of a recent edition of a 
4 Text-Book on Mental Diseases,” by Dr. Bevan Lewis. 


general paralysis ” proven; but I do think that all the 
evidence is in favour of the strong influence of syphilis in 
the production of general paralysis and the closely allied 
pathological condition tabes, and will now bring forward 
my reasons. 

(1) General paralysis is unknown where syphilis is un¬ 
known. In Iceland the only case ever seen was a syphilitic 
foreign sailor. Syphilis is extremely common, however, 
in Mohammedan countries and in Japan, hut general 
paralysis is rare. Some time ago, there were only 2 per 
cent, of general paralytics in the Asylum at Tokio, hut it 
must he remembered that the influence of civilisation has 
yet to he felt in Japan. In Mohammedan countries lunatics 
are looked upon as holy men and are usually free, there 
being only one asylum in Egypt. Comparing the insane in 
Egypt (a few years ago) with those in England, Dr. 
Warnock wrote to me :— 

“I should say syphilis is more frequent here. As to the 
frequency of general paralysis it is not so common as in England, 
but does occur. I have nine male general paralytics and three 
female now in hospital, besides two male syphilitic cerebral cases 
closely simulating general paralysis, which would be called that 
by some observers; this out of a population of 450. Of the nine 
male general paralytics three came from villages, four came from 
Cairo and one each from the large towns of Tanta and Zifta. 
Of the three female general paralytics one came from Cairo and 
two came from villages. The occupation of the men were: 
labourers, two; sailor (on Nile), one; tobacconist, one; servant, 
one; clerk, one; glass seller, one; unknown (probably labourers), 
two. Of the general paralytics all are Egyptians except one, 
a Syrian (white, like a Turk in type), and one general paralytic 
is a Berbery from Upper Egypt (reddish-brown skin, small 
featured). I have never seen a Soudanese (black) general 
paralytic. Now as to evidence of syphilis among these nine 
male and three female general paralytics. Of the nine males 
six have marks or history of syphilis, one is undoubtedly 
syphilitic, one has no signs of syphilis, but no history is obtain¬ 
able, and one (the Syrian) has no mark or history of syphilis, but 
it is noted that his father had syphilis. Of the three female 
general paralytics I can get no history nor find any marks of 
syphilis. None of them are prostitutes, and one developed 



general paralysis daring pregnancy. I have seen several female 
general paralytics here, bat none with marks of syphilis, though 
among the prostitutes here syphilis is, of course, common 

(2) In the rural districts of Ireland and Sweden, where 
alcoholism is common but syphilis rare, general paralysis is 
either extremely rare or unknown. 

(3) Priests, Quakers and clergymen are extremely seldom 
affected with general paralysis, and syphilis is also corres¬ 
pondingly rare. 

(4) In rural districts general paralysis is uncommon, 
likewise syphilis. The nearer we approach a large town the 
more common both become; probably the other factor, 
mental stress and the struggle for existence, is also greater. 
During the last twenty years I am informed that syphilis 
has increased in rural districts in Germany, and this could 
be accounted for by the compulsory military service, barrack 
life and syphilisation. 

(5) Syphilis affects all classes of males from peer to 
artizan, likewise general paralysis, but is common only 
amongst the lower classes of women, and diminishes as the 
station of life rises until it becomes very rare among the upper 
classes ; so also general paralysis. Examples have occurred 
of married couples suffering with syphilis, and of both de¬ 
veloping general paralysis. The proportion of males to 
females in asylums is 4—6 to 1. 

(6) In proportion to the reliability with which a history 
of syphilis can be obtained, so the authorities on the subject 
have been influenced in their opinion of the relation of 
syphilis to general paralysis. Thus, in Scandinavian countries 
where people suffering with syphilis are treated in a State 
hospital, where the history of previous infection can always 
be obtained, the relation of syphilis to general paralysis is 
not doubted. Kjelberg, Esmarck, and Jessen were the first 
to point out this connection. Fournier, who at first believed 
there was no connection between these two diseases, now 
teaches the doctrine that general paralysis and tabes are para- 
syphilitic affections. The most conclusive evidence has been 
afforded recently by the work of Hirschl, and the experience 


of Dr. Savage, Dr. Urquhart, 1 Dr. Conolly Norman, and of 
Dr. Ferrier fully accords with the view of the causal con¬ 
nection of syphilis and general paralysis. The following 
table of percentages in different countries will demonstrate 
what I have said. 

Asylum experience in England is continually brought 
forward as evidence against this doctrine. I have come to 
regard this evidence of very little value for the following 




Percentage of Syphilis 
in Paralytics. 





In Women. 



30 to 46 

n ii 


Westphal, A. 


ii ii 




n »i 


Sioli . 


ii >i 




i* ii 


Idanow .; 


ii n 



Percentage of Syphilis 
in Paralytics. 

of Syphilis 
in other 






11-6 to 12*7 






Bjorn strom 






Fiirstner .. 

32 to 40 


Lange . 

33 to 51 







33 to 45 


Ascher . 







Renand . 




40 to 72 





J acobsen 

43 to 52 






45 16 to 60 









50 to 64 


1 Dr. Urquhart has kindly forwarded me statistics showing the influence 
of syphilis, alcohol, and stress in the production of general paralysis among 
the middle classes in Scotland. Of twenty-seven cases there were thirteen 
undoubtedly syphilitic, eight probably syphilitic, four doubtfully syphilitic, 
two probably not syphilitic. 





Percentage of Syphilis 
in Paralytics. 

. of SyphUis 
in other 



50 1 



50 , 





Jastrowitz .. 









De Senna .. 






Peterson .. 

60 to 70 





Dietz . 













Hirt . 



Bonnet .. .. .. > 

66*6 to 80*2 


Bannister .. 

72 to 88 


Spillman and Dengler .. 

72 to 89 


Sokolowski .. .. , 

73 to 83 1 



73*3 to 80 


Cuylita .1 



Snell . 








75*7 to 86*9 




77 2 



77*2 to 76*8 


Geill . ! 



Rumpf . 






Savage . j 


50 i 

Anglades .. 

81*8 to 93*4 

51 1 







Dengler. ! 



R6gis . j 


According to Hirschl, syphilis occurred certainly in 56 per cent., probably in 
25 per cent., making 81 per cent, in all. His statistics relate to 200 cases. 

reasons : The most obvious syphilitic residua have been over¬ 
looked in the notes, the time occupied by the medical officer 
in taking notes of his 500 cases is necessarily limited, the 
history of syphilitic infection is obtained by sending out a 
printed notice to the friends to fill up. Most do not know 
the meaning of “venereal disease,” others will not acknow¬ 
ledge it if they do. In proportion to the time and care 
which is devoted to a careful enquiry into the antecedents of 


the patient, the signs and symptoms presented and the 
history of miscarriages and dead children in the women, 60 
the relative proportion rises. A study of Mr. H. W. Lewis’s 
paper is a striking confirmation of the above statement; 
moreover, the statements of Dr. Jones and Dr. Wiggles- 
worth, already alluded to, are strong supports to this 

Out of ten cases which I have seen at Charing Cross 
Hospital of general paralysis in the early stage in seven 
I obtained a reliable history of syphilis. At Claybury 
Asylum I am unable to see all the new cases, but I recently 
have made it my business to interview the friends of all 
patients deceased, and so far as it goes, I have been struck 
with the relative frequency of a probable syphilitic history 
in general paralysis as compared with other forms of 
insanity. In 40 cases of general paralysis of which I have 
notes, 60 per cent, had certainly had syphilis. In 10 per 
cent, acquired syphilis could almost certainly be excluded. 
Moreover, syphilitic residua are much more frequently 
found on the body post mortem than in other forms of 
insanity, excluding brain syphilis. 

(7) It is a fact that a great many cases of general 
paralysis and tabes have suffered with what was believed to 
be a soft sore. Many of these cases were undoubtedly 
syphilis, modified possibly by previous infection of ancestors, 
possibly by mixed infection, and some were the true soft 

Most authorities recognise that syphilitic residua are 
found in only a certain proportion of cases of general 
paralysis. Evidence of tertiary lesions is certainly not 
common. It is therefore contended that syphilis cannot be 
the cause of the disease and that it is a mere coincidence 
that the patient has had syphilis, seeing that it is so 
prevalent. Moreover, if syphilis is the cause, why do not 
anti-syphilitic remedies afford relief and arrest the disease ? 
for undoubtedly it is very rare that either mercury or iodide 
or the two combined have any influence upon general 

Frequently the mild cases are untreated; the poisons 



may, as Hitzig states, be several, some of which have a 
toxic influence upon the nervous system, or poisons may be 
produced in the blood by the infection which in an insidious 
manner act upon the specific vital energy of the neuron, caus¬ 
ing, under the influence of stress or inherited predisposition, 
early decay, which, when once started, cannot be in any 
way remedied by anti-syphilitic remedies, for the degenera¬ 
tive process that is set up at a late period after infection is 
not due to an active syphilitic poison, but to the devitalising 
influence of the poison after infection. An analogy is found 
in diphtheria. 

(8) General paralysis is generally admitted (and it is 
certainly my experience) to be due less to heredity than 
other forms of insanity; it is, in my opinion, an organic 
brain disease with mental symptoms. 

(9) The fact that a previous history of syphilitic infection 
cannot be obtained in a certain proportion of cases depends 
upon the class of patient and many other conditions, but in 
a great many cases of obvious tertiary syphilis of the ner¬ 
vous system, of the skin, the bones, and the viscera, no 
history of infection can be obtained; yet the physician is 
sure from experience that the disease is due to syphilis in 
spite of the patient’s denial, and confirmation is afforded by 
the success of treatment. In at least 20 per cent, of obvious 
syphilitic skin lesions, Crocker found no history of infection ; 
therefore, to say that general paralysis^ or tabes cannot be 
due to syphilis unless in every case a history can be obtained 
is absurd. Women often are infected and have no charac¬ 
teristic lesions; frequently, no doubt, they are immunised 
by a spermatically infected foetus; so that they have the 
disease so mildly that it is not recognised by any notice¬ 
able impairment of health. 

(10) In a recent paper 1 from the West Riding Asylum by 
Dr. Simpson it is contended that syphilis cannot play any 
part in the production of general paralysis, for he met with 
extremely few cases of recent infection or secondary rashes. 
This is the experience of all asylum authorities, but I would 
rather believe with Krafft-Ebing that this is an argument 

1 “ Journal of Pathology.” 


in favour of the intimate relation of syphilis to general 
paralysis; for, considering the very promiscuous sexual life 
these people lead in the early stages of the disease, the 
fact that they do not present evidence of recent syphilis is 
a convincing proof that they are immune to the disease by 
previously acquired or inherited infection. Krafift-Ebing 1 
has put this to the test; he has inoculated eight general 
paralytics with the virus of a typical hard chancre, and 
observed them carefully during a prolonged period more 
than 180 days ; the cases selected were men who presented 
no signs of syphilis on the body, yet not one of these mani¬ 
fested any syphilitic phenomena—a striking proof that they 
were immune by acquired or inherited infection. 

(11) Oppenheim, in the recent edition of his text-book of 
neurology, regards the above experiment as a crucial test, and 
he states that a person who has not had syphilis, but who is 
the subject of mental stress and excitement and excesses in 
baccho et venere, is liable to develop neurasthenia; the 
syphilitic neurasthenic, however, is liable to dementia 
paralytica. This seems to be the correct explanation of the 
process: it is the outcome of stress and syphilis. That stress 
plays an important part appears to be shown by the relative 
weights of the hemispheres (vide pp. 183-185). 

(12) Perhaps the most conclusive proof in support of the 
view that syphilis is the most important factor in the pro¬ 
duction of general paralysis of the insane is afforded by the 
study of those somewhat rare cases of the juvenile form of 
the disease to which I have given special attention, and to 
which I refer the reader for further information. It seems 
to me to show that even stress is of less importance than 
syphilis, although it by no means excludes this as an excit¬ 
ing factor in the disease. It will be observed that in my 
report of twenty-two cases occurring in the London asylums 
the sexes are equally affected, because the chance of infec¬ 
tion by inheritance is about the same; whereas in the 
acquired form males are much more prone to infection than 
females (p. 250). 

1 “ Discussion on General Paralysis,” International Congress, Moscow, 
1897. Ref. Neurol. Ceutralblatt, 1897. 



Association of General Paralysis and Tabes. 

I consider that general paralysis and tabes are, patho¬ 
logically speaking, the same disease, affecting different 
portions of the nervous system; but I know of one distin¬ 
guished neurologist and alienist who holds that this cannot 
he, because tabes is of a syphilitic origin and general paralysis 
is not. Out of twenty-eight cases of tabes that I have seen 
in my hospital practice in twenty-four I obtaiued a definite 
history of syphilis. In one of these cases, in which I did 
not obtain a specific history, the patient subsequently 
developed general paralysis, and I obtained a most definite 
history of syphilis from his brother, when he came to view 
the body after death. In very few of these cases of tabes 
was the syphilitic infection of a severe nature, and the 
majority presented no obvious residua in the skin, glands, &c., 
in that respect agreeing with general paralysis. It has, 
however, been argued that the lesion in tabetic general 
paralytics is of a different order to that of ordinary locomotor 
ataxy. This is not my experience. In conjunction with my 
assistant, Dr. Wright, I have examined the spinal cords of a 
number of cases of the tabetic form of general paralysis, 
and in all these cases the lesion is essentially one of the 
exogenous systems of spinal neurons, combined with the 
characteristic changes met with in the brain, viz., pia arach¬ 
noid thickening, granular ventricles, disappearance of the tan¬ 
gential system of fibres combined with atrophy of the cortical 
cells. I think, therefore, that those authorities who admit 
the very important role played by syphilis in the production 
of tabes should also admit it for the allied disease, general 
paralysis, especially when it is remembered that by far the 
most frequent and the most important early physical sign of 
both diseases is the rigidity of the pupil to light while accom¬ 
modation persists. In no other condition, except brain 
syphilis, by reason of its frequency, do we find this phe¬ 
nomenon form an important diagnostic symptom. Again, 
there is a striking similarity in the paroxysmal character of 
crises of pain and visceral disturbances of tabes on the one 
hand, and the congestive, epileptiform and apoplectiform 


seizures of the allied disease on the other hand. Both 
probably indicate the increased irritability of decaying 
nervous structures. 

In the large number (over fifty) of spinal cords I have 
examined of persons dying of general paralysis, I have 
invariably found in the spinal cords of those patients who 
have for some time prior to death been the subject of 
epileptiform seizures a large number of degenerated fibres 
in the direct and crossed pyramidal tracts. Elsewhere, in 
the lateral columns, I have found little or no degeneration, 
and I now am able to predicate, more or less, degeneration 
and sclerosis of these systems if the patient has been the 
subject of epileptiform seizures during the course of hiis 
illness. These fibres show degenerative changes because 
the cortical pyramidal cells of which their axons are the 
prolongations are either dying or dead. It may be the same 
in tabes, vide Case 27, in which an out-patient of mine had 
optic atrophy and exaggerated knee-jerks, but he was 
suffering with lightning pains. I predicated that probably 
when he again came the knee-jerks would be abolished, for 
the shooting pains in the legs were an indication to me that 
the posterior roots were being destroyed, and that the 
afferent portion of the reflex circle would soon disappear. 

Again, the case examined by Mr. Salaman showed how 
profoundly the roots of the dorsal (visceral) region were 
affected, the lumbo-sacral much less. This patient, a 
woman, was the subject of gastric crises and mental 
symptoms. Cases of tabes with mental symptoms are met 
with in asylum practice, and we may divide them into the 
following classes : (1) Those which commence with tabes, 
mental symptoms supervening later; (2) those which com¬ 
mence with mental symptoms (mental crises), and later on 
develop symptoms of tabes; (3) both conditions associated 
simultaneously. The pathological process is identical, to 
my mind, in all these cases, and many of them would 
be called at one period of their existence tabes, at another, 
tabetic general paralysis. 1 Qrey atrophy of the discs is 

1 For want of space I am obliged to omit in this volume the account of a 
number of cases of tabes, and of the tabetic form of general paralysis; but 
these will be published in the next volume. 



frequently present in cases of the tabetic form of general 
paralysis, and one can generally find in such cases 
atrophy of the exogenous afferent system of neurons, 
when the cord is examined. Mobius, 1 who has devoted 
an immense amount of thought to this subject, and has a 
large experience thereon, looks upon both diseases as 
metasyphilis, and concludes that they are one and the 
same disease affecting different parts of the nervous system ; 
and I must say that the more I work at this subject, both 
clinically and pathologically, the more convinced I am of 
the truth of the doctrine of the unity of the affections. 

Congenital Syphilis in the Children of General Paralytic 
Fathers .—In the study of some cases of congenital syphilis, 
I came upon a patient who had been in Charing Cross 
Hospital, under Dr. Abercrombie, for attacks of vomiting. 
It w'as one of the most typical cases of congenital syphilis 
that could be found, the linear scarring around the mouth 
being very marked; moreover, there was a maternal history 
of miscarriages and stillbirths. I subsequently found this 
child was under the care of my friend, Dr. Taylor, Superin¬ 
tendent of Darenth Asylum, and he asked me to see her. 
I found she had absent knee-jerks, pupils dilated and fixed 
to accommodation and light, commencing grey atrophy of 
discs, and she is still suffering with spasmodic attacks of 
vomiting (gastric crises). I have no doubt there is in the 
patient an atrophy of the first exogenous afferent system 
of neurons in the dorsal region. The interesting point, how¬ 
ever, is this. I heard that the father was in Banstead 
Asylum, and therefore wrote to Dr. Claye Shaw for infor¬ 
mation ; he kindly replied that the patient was dying of 
general paralysis, but there were no signs of syphilis on the 
body.* He has, however, left the taint well marked enough 
in his offspring. Among the twenty-two cases of juvenile 
general paralysis there were three out of twenty, in which 
there was a history of the father having died of general paraly¬ 
sis. In the light of the above case, we may consider that, as 

1 Ueber die Tabes. 

s Since writing the above the man has died and the characteristic lesions 
of the brain were found at the autopsy. 


the offspring in two cases showed definite signs of congenital 
syphilis, they derived the specific taint from the father, and 
the syphilitic poison was therefore probably concerned not 
only in the degenerative process, which was fatal to the 
children, hut to the father as well. In the other case, 
A. B., there were no signs of syphilis on the body, but the 
maternal history strongly supported the view that it was 
of syphilitic origin. The fact that the sexes are equally 
affected in the juvenile form, because the chances of syphi¬ 
litic infection are about equal, is a striking corollary to the 
fact that in the adult form males are affected much more 
frequently than females. 

Syphilitic residua, in the form of scars, enlarged glands, 
pigmentation of skin, old iritis, scars of chancres, are not 
met with in the majority of cases of general paralysis ; but 
excluding brain syphilis they are enormously more frequently 
seen on the post-mortem table in general paralysis than in 
the other forms of insanity. The statistics I append 
strongly support this statement. 

General paralytics, as a rule, show no stigmata of 
insanity; they are usually prior to their illness mentally and 
physically well-developed, and one would predicate the 
development of the disease rather from their personal than 
from their family history. 

Since I have made all the post-mortems at Claybury, I 
have made the following statistics :—From September, 1898, 
to May 14, 1899, out of seventy-six males thirty-nine were 
aged 50 years or under, and of these twenty-five were 
general paralytics, two had syphilitic brain disease and 
twelve had non-organic brain affection. Six general para¬ 
lytics had positive signs of syphilis, nine had doubtful signs, 
ten had no signs. The signs relied upon were scar on the 
penis, pigmentation of the skin, scars or rashes, enlarged 
glands, &c. The two syphilitic cases had marked signs, the 
twelve other cases of non-organic brain affection had no signs. 

There were forty-two females under 50 years, seven were 
general paralytics; none of these had positive signs, two 
had doubtful signs and five negative. This is in accordance 
with what we know of the slight residua of syphilis in women. 




Atheroma of the aorta and endarteritis cerebri are 
much more frequently met with in general paralysis than 
in other forms of insanity, excluding syphilitic brain disease. 
It is remarkable, however, that I have not found in any 
of the cases of juvenile general paralysis endarteritis cerebri, 
although usually there were some slight fatty changes in the 
deeper sub-endothelial cells of the aorta in most cases. 

Mental activity, stress in the struggle for existence 
among people who work with their brains rather 
than their hands, is another important factor. The 
striving, ambitious, sexually excitable, town-bred in¬ 
dividual suffering with brain fag (encephalasthenia) is 
especially liable to develop general paralysis if he has been 
infected by syphilis, and possibly it may develop after 
influenza. According to Hirschl, other infectious diseases 
play no part in the etiology, although various authorities 
have brought forward cases which seem to show there is 
association between the onset of the disease and some 
previous infectious complaint. 

A patient was sent to me at Charing Cross Hospital 
with well-marked signs of general paralysis, which the 
doctor said came on after influenza; but in which there was 
a history of syphilis with obvious residua. No doubt the 
influenza acted as one factor, but it is questionable whether 
it would have produced the disease if the man had not 
previously had syphilis. 

It is argued that mental activity cannot play much part 
in the majority of the cases of general paralysis among our 
pauper lunatics of large towns. A history of these people 
shows that, although they were labourers, artisans, &c., they 
were, as a rule, quick-brained individuals. The argument, 
because they were in a low station of life that their mental 
activity was not great, does not hold at all. The reaction 
time of a London ’bus-driver is as quick, if not quicker than 
the most intelligent professional man, and the vocabulary 
of a low-class cockney is as much greater than that of a 
coqntry labourer as is the facility with which he can make 
use of it. The mental activity of the lower class urban 
population is immeasurably greater than that of the 


country labourer, and I believe this is one of the reasons 
why general paralysis is more prevalent in towns than 

The history of juvenile general paralysis shows the im¬ 
portant part played by mental activity in the development 
of the disease. In many of the cases {vide pp. 250-320) the 
disease developed just after puberty, at a time when new 
emotions, passions, ambitions and disappointments, asso¬ 
ciated with the awakening and development of the sexual 
instinct, originate a new psychical existence, wide-spreading 
cerebral activities and increased bio-chemical change. 

The dictum of Virchow upon which modem pathology 
is based, “that a cell nourishes itself and is not nourished," 
should be the key to the explanation of the pathological 
process which underlies this disease. Let us start with 
certain premises: (1) The neuron is a complex branching 
nerve cell. (2) The neuron is the essential nervous ele¬ 
ment. (3) The whole nervous system is made up of these 
anatomically independent, but physiologically interdepen¬ 
dent nervous units. The nervous units decay and die be¬ 
cause they are unable to assimilate from the lymph 
environment the material necessary to repair the waste 
occasioned by the bio-chemical changes incidental to their 
aroused vital activities. The morbid process is essentially 
one of defect of specific vital energy of the neuron itself, 
although subsequently vascular complications may arise 
which will lead to traumatic death of neurons and estab¬ 
lishment of a vicious circle. That mental stress does play 
a part in the development of the disease finds anatomical 
support in the greater wasting of the hemisphere which is 
most used (vide pp. 183-186). This also supports the view 
that the change is primarily parenchymatous, but that 
secondary destructive changes do occur, the result of 
ineningo-encephalitis and the establishment of a vicious 
circle (i ride pp. 190-195). 

The Reproductive Organs. 

Sexual excesses are rightly believed to lead to neuras¬ 
thenia, partly by violent emotions and exhaustion of the 



nervous system; but it may also be by the loss to the body 
of highly complex phosphorous compounds. The idea of 
Brown Sequard, that injection of testicular fluid would be of 
benefit in neurasthenic conditions, although it led to a most 
important development in the injection of other animal 
extracts, has not met with success. Yet there is much to 
be said in favour of the theory that loss of spermatic fluid 
by sexual excess and masturbation may cause a loss to the 
body of important complex chemical compounds difficult to 
replace in the blood, but of which a fall below the physio¬ 
logical minimum may mean depriving the nervous system 
of some substance essential for its metabolism. The fact 
that male general paralytics run a more rapid course than 
female may find some explanation in this theory. The 
profound effect upon body and mind of castration, and 
thereby removal of the internal secretion of these organs, has 
been known from time immemorial. Again, the wasting of 
the testicles in general paralysis is often out of proportion 
to the wasting of other organs. Lastly, the infantile de¬ 
velopment of the reproductive organs in the juvenile form, 
the absence of spermatozoa in the testicles, and the degenera¬ 
tive changes; also the cessation of menstruation and the 
degenerated appearances presented by the ova and the 
ovaries, all suggest an important functional relation 
between the reproductive organs and the whole nervous 
system {vide pp. 250-320). 

Alcoholism is considered by many authorities as an im¬ 
portant factor in the production of general paralysis. It 
does not directly play any part in the juvenile form of the 
disease ; still, we know that a toxic agent such as alcohol in 
certain individuals can cause degenerative changes in the 
neuron, even in the tangential system of fibres (vide p. 518); 
but the difference between the effect of alcoholic intoxication 
and the syphilitic poisoning is that the former is proportional 
to the dose; and if the poison is removed the progress of 
the degenerative change may be arrested also, and even 
function restored; whereas in general paralysis the decay is 
progressive and cumulative. Mr. Lewis’s cases do not show 
that intemperance was a very important factor. However, 


I cannot help thinking that alcohol is a most powerful agent 
in assisting the toxic influence of the syphilis, for so many 
of the cases of juvenile paralysis give a history not only of 
syphilis in the father, but also of alcoholic intemperance. 
Again, syphilitic brain disease is so frequently associated 
with a history of alcoholism that there must be a causal 
relation. There can be no doubt that alcoholic abuse in the 
early stage of the disease greatly accelerates the progress of 
the malady. Some of the most rapid cases are those that 
are admitted into the asylum with mania a potu; and 
mania in a man between 30 and 50 which lasts more than a 
month after all chance of obtaining drink is removed is 
usually the mania of general paralysis. A neurasthenic who 
had had syphilis, and who resorted to drink in order to give 
a temporary fillip to an exhausted nervous system, would 
undoubtedly thereby add to the chances of nervous ex¬ 
haustion terminating in organic disease. 

The manner in which the evil results of alcohol manifest 
themselves depends very much upon the motives which lead 
to drinking. I consider alcohol is especially toxic to the 
neuropath and the neurasthenic, who drink to stimulate an 
exhausted nervous system, and succumb through the effects 
of the poison on the nervous system before there is time for 
grave organic changes to occur in the liver, and this explains 
why I seldom see in the post-mortems made at the asylums 
hobnailed liver and ascites. The only really marked case I 
have seen in a large experience was the case of a woman 
well known in the London police courts, but who was con¬ 
victed nearly 400 times for drunkenness before it was found 
possible to certify her as insane and incapable of taking care 
of herself. Yet we know that a large proportion of the cases 
which are admitted into the asylums are due to drink. 
Probably the reason why those people have not cirrhotic 
livers is that the toxic influence of alcohol upon the nervous 
system in these hereditary neuropaths is much greater 
than drinkers with initial mental stability who attend our 
hospitals, where cirrhosis of the liver is common enough. 
Consequently neuropaths who drink, suffer early by the toxic 
influence upon the nervous system, and thus they are unable 



to take alcohol in sufficient quantity, or for a sufficiently 
long time, to produce cirrhosis of the liver before they are 
certifiable lunatics. According to my experience, there are 
two important preventible causes of insanity, and they are 
syphilis and alcohol, and the more I work at the subject the 
more evident this fact becomes. 

Pathology of General Paralysis. 

In discussing the pathology of this disease I shall refer 
to investigations which have been made upon the nervous 
system, the muscular system, the circulatory system, the 
blood, and some of the viscera. A few selected cases are 
published in abstract at the end of this chapter, and also 
a special article on the juvenile form of the disease, with 
notes of twenty-two cases. 

The Nervous System. 

The brain atrophy, independent of coarse vascular lesions, 
is by far the most striking objective phenomenon in general 
paralysis; it affects especially the frontal and central regions 
of the hemisphere, and spares as a rule the occipital tem¬ 
poral lobes. The atrophy affects especially the hemispheres, 
for the normal weight of the pons, cerebellum and medulla 
is diminished much less than that of the hemispheres. On 
weighing the hemispheres of some juvenile general paralytics 
I was struck by the fact that the left hemisphere weighed 
invariably less than the right. I therefore took precautions 
to weigh (after carefully draining) the two hemispheres in 
all patients that died at Claybury Asylum since September 
1st, 1898. I shall first only, however, compare the relative 
weight of the two hemispheres in patients under 50, thereby 
eliminating cases of cerebral softening from vascular oc¬ 
clusion. I shall also not include cases of tumour or obvious 
macroscopic brain disease. 

In all doubtful cases a microscopical examination was 


Non-General Paralytic Cases , includ¬ 
ing Epilepsy , Alcoholic Dementia , General Paralytic Cases . 

Melancholia , Afania. 

28 Cases. 24 Cases. 

(1) Right heavier, 9 cases .. 32% (1) Right heavier than left, 15 

Average difference 8*3 grins. cases .62*5% 

5 men. 4 women. Average difference, 23 grms. 

12 men. 3 women. 

(2) Left heavier, 2 cases .. 7% (2) Left heavier than right, 3 

1 man; 1 woman. 7 grm. average. cases .12*5% 

2 men. 1 woman. 15 grms. 
average difference,, 

1 left-handed person. 

1 woman. 33 grms. difference. 

(3) Right equal to left, 17 cases 64% (3) Right equal to left, 5 cases.. 20% 

14 women. 3 men. 5 men. 

Juvenile General Paralysis . 

In 6 cases in each of these the right 
was heavier than the left, average 
28 grms. 

5 females. 1 male. 

It will be observed that these statistics show certain 
facts: (1) that in non-general paralytics the proportion of 
cases with the two hemispheres equal is more than three 
times that of the general paralytics; (2) that in general 
paralysis the proportion of cases of the right hemisphere 
exceeding in weight that of the left is more than double 
that of the non-general 1 paralytic cases, and if we add the 
juvenile cases and the left-handed person, the percentage 
in which the comparative diminished weight of the hemi¬ 
sphere which is used most in speech and all special manual 
operations is raised to 71 per cent.; (3) I have weighed a 
number of normal brains from people dying of pneumonia, 
heart disease, cancer, &c., and the two hemispheres exactly 
balance, also the hemisphere of two cases of Congo sleeping 
sickness, in which there was very marked leptomeningitis 
and encephalitis, which also exactly balanced one another. 
I consider this a strong support in favour of the argument 
that stress on those nervous tissues which are most in use 

1 Probably two of these cases were really general paralysis, certainly one 
of the males certified as mania had all the microscopical characters of 
general paralysis. 



is an important element in the production of the morbid 
process. At my suggestion my assistant, Dr. Wright, has 
pursued this study further, and the results of his obser¬ 
vations upon the relative atrophy of the tangential system 
of fibres in Brocas’s convolution of the two hemispheres 
supports this theory. I shall be more satisfied when a 
larger number of cases have been collected; but so far the 
results are worthy of record. 

Comparison of the weights of the hemispheres in 155 cases 
of patients of all ages, excluding cases with obvious soften¬ 
ing, tumours, dtc., dying in Clay bury asylum. 

Of seventy-seven male post-mortems, excluding eight 
gross lesions = sixty-nine, there were twenty-eight general 
paralytics: six with hemispheres equal; twenty with the 
right heavier than the left, the greatest difference being 
forty, the least three, average fifteen grams, difference; two 
with left heavier than the right, ten and fifteen grams, 
respectively. Of non-general paralytics there were twenty- 
one of equal weight; eight with the right hemisphere 
heavier than the left, average seven grams.; twelve with 
left heavier than the right, average nine grams. 

Out of eighty-six female post-mortems, gross lesions 
having been excluded, there were twelve general paralytics: 
seven with right hemisphere greater than the left, average 
twenty grams.; two with hemispheres equal; three with 
left hemisphere greater than the right, average eighteen 
grams. One of these was a left-handed person, whose right 
hemisphere weighed twenty-six grams, less than the left; 
another was a doubtful one, as it is called restless 
melancholia, but the post-mortem appearances are sugges¬ 
tive of general paralysis, and I have therefore included it. 
Of the non-general paralytics there were forty of equal 
weights ; nineteen with the right hemisphere heavier than 
the left, including all ages, average nine grams, difference; 
left hemisphere greater than the right fifteen, with an 
average of five grams. There were 24 - 5 per cent, general 
paralytics in the 155 cases analysed, and 75 5 per cent, non¬ 
general paralytics. 

*11 pp 


of the two hemisphere* ‘A a case .of genera) paraly-h* which bou«o 
tnoprhsh.efnr* with typical fcympunrj* of I&.eofn'ntot' ataxy. Tb* pattbht vyavsnb^tTerkfy' ftfiftlittil 
ihtn Cane Hill asvluih with marked speech affection. pro^r«i-.>oc dcnunjfcia. and other of 

genenii paralyses.. There was ft different 1 ot *.0 granmioVm the weight of the two h%?.ii»i*.phf-m*. 
A compMVJif.ivr- lAwwiii'^a of the frontal 'lobes- of the two hemispheres ‘tliov.r. a marked flatten mg 
of the 1* ft a-v compared with the right,: r>he .left third frontal and its )unction with the a-vVhdmg 
/rental X smaller and le«* vCftmlfiA than the right. Thfc tangential fibres have entirely dis 
appeared ob the left side iri Bfrit£fb$ coh\d)dt;icm but ace fftirlv nuaierouH mi-tite right shh 
F. \V . M, y-.* ■ : ’• ‘ 


Comparison of the Percentages of the General Paralytics and 
Non-Genebal Paralytics. 

General Paralysis. 
Right heavier than left .. 67*5 % 
1 Left heavier than right.. 20 % 

Eqnal .10 % 

Non-General Paralysis. 

Right greater than left .. 23*5 % 
Left greater than right .. 23*5 % 
Equal .53 % 

It will be observed that essentially the results are the 
same whether we neglect all cases over 50 or not. 

Chemistry of Degeneration. 

Some years ago I read a paper at the Neurological 
Society showing that there was evidence to prove that 
when nervous tissue underwent degeneration, protagon or 
lecithin broke up into ‘cholin, glycero-phosphoric acid and 
stearic acid. The Marchi reaction shows that the protagon 
is converted into a fat of a different composition. Chemical 
analysis of the degenerated half of a spinal cord, as com¬ 
pared with the non-degenerated, showed that the phos- 
phoretted fat had broken up into a simple non-phosphoretted 
fat which stained black by Marchi method. For further 
particulars vide p. 346. Examination of the brains of 
general paralytics by Marchi method often reveals evidence 
of degeneration, and in acute cases, or cases in which there 
have been prolonged epileptiform seizures, very numerous 
black degenerated fibres are seen. The black particles, 
moreover, may be seen in the perivascular lymphatic 
sheaths (p. 275), contained in leucocytes and endothelial 
cells, and Halliburton and I have shown that cholin may 
be obtained from the cerebro-spinal fluid after death, and 
also that it exists in the blood and cerebro-spinal fluid, of 
general paralytic patients, the subjects of epileptiform 
seizures during life. We must therefore assume that 
nervous degeneration such as occurs in general paralysis 
is associated with the escape of cholin into the cerebro¬ 
spinal fluid and blood {Abstract of Proceedings of the 
Royal Society, vol. 64 2 ). In the cerebro-spinal fluid there is 
also a great excess of nucleo-proteid. These experiments 

1 Left-handed person not included. 

r A full account of this research will shortly be published in the Philo¬ 
sophical Transactions of the Royal Society. 



afford a direct proof of auto-intoxication. Cholin is a 
toxic substance but not very powerful, it produces a fall in 
the blood pressure partly by slowing the heart’s action, 
but mainly by paralysing the peripheral neuro-muscular 
mechanism of the splanchnic arterial system. The ex¬ 
istence of nucleo-proteid and cholin in the cerebro-spinal 
fluid might tend to produce stasis in the veins of the brain, 
especially those opening into the longitudinal sinus, in 
which the blood flows contrary to gravity. 

The cerebro-spinal fluid not only contains cholin but 
also nucleo-proteid. Whether this, in contact with the wall 
of the veins, can induce a tendency to coagulation or stasis 
of the blood even, I do not know; but it is possible that it 
may have such an effect, seeing that if injected into the 
circulation it causes instantaneous coagulation. The cellular 
proliferation and the leucocytic accumulation in the lym¬ 
phatic sheaths of the vessels is always most marked where 
the cellular degeneration is most profound and recent; and 
it is possible that this inflammation is due to irritation 
produced by the products of degeneration. The only cases 
of thrombosis of veins which I have seen, now four in 
number, have occurred in the large veins opening into the 
longitudinal sinus. The blocking of the vein in the cases 
examined was due to acute inflammation of the wall of the 
vessel {vide case G. M., p. 199), and I have seen two cases of 
pachy-meningitis haemorrhagica, both of which I found due 
to rupture of the wall of an inflamed vein—the veins of the 
brain have no muscular fibres in their coats; they consist 
of an adventitia lined by endothelium, and the large veins, 
which open into the longitudinal sinus, often run for an 
inch or so in the substance of the dura mater before opening 
into the sinus in a direction opposite to that of the current. 
The “ chord® Willisii ” in the sinus and in these sinusoidal 
veins would facilitate stagnation of the blood, and this 
would occur very much more frequently than it does were it 
not for the fact that the great anastomotic vein is connected 
by a large vein with the lateral sinus, so that obstruction 
in the longitudinal sinus finds a relief by this connec¬ 
tion. Reference to the diagrams (figs. 1 and 2) shows that 


They shading xhuivu tho arm of pi# amchtttrid tWctoaiing. A i&,rg& 

brMudj ik «%^ti thonhig Mdfc ioio ihn ifeitfrnY svngtei connecting it with the 
grfcat tieriiml auastornotiV vein. The iatflfttl simja is diagrammatacaiiv reprt> 
acufced as continuous with the longitudinal m-Mk, and the torcula, i$ noijfamf. 

«eui? opening into the longitu 

dlnal kinvx dm'iniwg' tjinr upper portions whtr^ the thidke&jft# of the pi a 
arachnoid ocenrs. Only a vhmiJ portion of the Uu^ia^dn.Hi *ino* is* r»3prfe- 
rented.' Theso dialing* an* .fem thd 'RVeA of- pi« 

•arachnoid thickening And it* corvospoudcucv \h y;r<at. measure «Vtih the urea 
drained by v^ina opening into ih# long^jdmcd ‘ ' ' 'vy> : V.Y.;. 




the parts of the brain which usually exhibit thickening and 
opacity of the pia-arachnoid membranes coincides more 
closely with the distribution of the veins opening into the 
longitudinal sinus than with the distribution of the internal 
carotid artery, for it will be observed that the gyrus forni- 
catus, which is supplied by the anterior cerebral, usually 
escapes, and the under surface of the orbital convolutions; 
whereas the mesial surface of the frontal lobe, the tip of the 
temporo-spbenoidal, the anterior two-thirds of the upper and 
outer surface of the hemisphere, and the mesial surface of the 
hemisphere in its upper part, usually show pia-arachnoid 
thickening, and this corresponds with the distribution of the 
aforesaid veins. I have noticed this pia-arachnoid thicken¬ 
ing also in epileptic dements ; moreover, these veins are 
especially congested in cases of general paralysis with 
epileptiform seizures and in cases of status epilepticus. The 
circulation of the blood in the veins of the brain depends 
upon two forces, the vis a tergo and the vis a fronte ; the 
latter is an important factor and depends upon the suction- 
pump influence of the heart, but more especially upon the 
negative pressure in the thorax during inspiration. During 
the tonic spasm of the expiratory muscles, this negative 
suction influence is abolished, and there will be venous 
congestion; when the suction influence is brought into action 
it will make itself felt first in draining away the blood from 
those veins which open directly into the lateral sinuses and 
the torcula herophili ; consequently those veins which 
drain into the longitudinal sinus and in which the flow is 
against gravity will suffer the most from congestion, as they 
will be the last to be relieved by the mechanical influences 
which determine the flow of blood from the brain. 

Thus, we see there are two reasons why the area of 
distribution of these veins should be the seat of this pia- 
arachnoid thickening; two conditions which mutually in¬ 
teract upon one another in the establishment of a vicious 
circle, viz., degenerating nervous structures, the degenerated 
products of which accumulate and irritate the peri-vascular 
lymphatics surrounding the veins, causing a tendency to 
stasis and inflammation, combined with conditions which 


produce mechanical congestion in the veins; and this 
reacting back on the nerve structures leads to still further 
disintegration of nervous tissue: thus the one vicious 
condition feeds the other. 

(Edema of the brain, owing to dilatation of the peri¬ 
vascular lymphatics, is a striking feature in general paralysis, 
and the water which can be extracted from the brain by 
placing it in a desiccator is larger in amount than in the 
normal brain (see Dr. Barratt’s paper, p. 214). But venous 
congestion and oedema of the brain must be associated 
with arterial anaemia, for the brain being in a closed cavity, 
the amount of arterial blood is proportional in a measure to 
the space occupied by venous blood. More venous blood 
means less arterial. The capillaries of the brain are in a 
state of inflammation, and the flow through them is hin¬ 
dered. If all the arteries to a dog’s brain he ligatured, there 
is established an arterial anaemia, but the veins of the cortex 
will be found greatly congested, the peri-vascular lymphatics 
distended, and the motor cortex excitable, even hyper- 
excitable to electrical stimulation. This will be dealt with 
further in a paper on Status Epilepticus (see p. 493), but it 
makes it probable that the epileptiform seizures of general 
paralysis are associated with and probably dependent upon 
venous congestion and stasis, arterial anaemia and increased 
excitability, which, starting perhaps from a minute area 
where the venous stasis is most profound, sets up a focus 
of excitation which spreads to other areas, causing death of 
a certain number of the pyramidal neurons of the motor 
efferent system proportional to the length and severity of 
the seizures. Examination of the spinal cords in fifty cases 
of general paralysis has shown me, that in those cases where 
there have been for some time prior to death prolonged 
epileptiform convulsions, one can with certainty predicate a 
proportional recent degeneration of the fibres of the pyramidal 
system in the spinal cord. The fact that seizures can be 
cut short by a purgative or an enema supports this view of 
the importance of venous congestion, for we know that this 
relieves the portal system and thereby relieves congestion of 
the whole venous circulation. 



In starvation and wasting diseases the brain hardly loses 
any weight; this would seem to indicate either that in the 
normal functional activity of the brain only comparatively 
slight metabolic changes occur, or that the brain is preserved 
while the less important tissues suffer. I have recently seen 
some striking examples of this, e.g., in a case of Congo 
sleeping sickness, a boy aged 10, there was the most profound 
emaciation, the whole body weighing less than 3 stone, and 
yet the brain weighed 36 oz. Another case of septicaemia, 
with continuous pyrexia, varying from 100° to 103°, in 
which the body weight fell from 13 stone to 7 stone, 
and in which there was the most profound anaemia, the 
result of haemolytic processes and haemorrhages; yet the 
brain presented the normal appearance and weight, and 
microscopically the cells of the central nervous system 
presented no abnormal characters when stained by the Nissl 
method (vide plate ix., photo. 1). Likewise in two cases of 
pernicious anaemia, in which there were the most profound 
haemolytic changes, and the characteristic appearances met 
with in the red marrow, together with deposition of free 
iron in the liver, no changes could be observed in the nerve 
cells (vide plate v., fig. 1). 

In many cases of general paralysis, which die from com¬ 
plications during the first and second stageB of the disease, 
the body is well nourished and the organs apparently healthy. 
Moreover, as Mr. Green’s observations on the blood show, 
the number and character of the corpuscles are normal or 
nearly so; and yet in these cases the brain usually shows a 
marked atrophy of certain parts; we must therefore assume 
that the disease is primarily cerebral, and if changes in the 
other organs of the body occur, indicating defective meta¬ 
bolism, they are secondary to changes in the nervous system. 
I have already indicated my reasons for supposing that the 
disease is aprimary degeneration of the neuron, with secondary 
inflammatory changes, that is to say, it is essentially a 
parenchymatous degeneration due to a loss of durability of 
the nerve cells—a premature decay of tissue in which in¬ 
herited and acquired conditions take part with the result 
that progressive death of the latest and most highly de- 


veloped nervous structures ensue as soon as their vital 
energy is unable to cope with the antagonistic influences of 
environment. All the tissues of the body are interdependent, 
and no one can suffer without affecting the rest. Bapid 
destruction of the brain may, we have seen, give rise to 
auto-intoxication, local and general, and the process of decay 
may be progressive and cumulative, and lead to the establish¬ 
ment of a vicious circle which is continually enlarging. The 
congestive, epileptiform and apoplectiform seizures of 
general paralysis are coincident with either auto-intoxication 
or primary destruction of brain tissue,—they may be accom¬ 
panied, even in their earliest stage, by pyrexia. The fever 
usually rises considerably during epileptiform convulsions; 
it may be due to increased thermo-genesis from clonic and 
tonic spasms of the muscles, for I have found usually that 
the surface temperature is a little higher, perhaps as much as 
half a degree (when the convulsions are unilateral), on the 
side which is undergoing contraction, than on the other 
side; and the fever is proportional to the severity of the 
convulsions (vide cases p. 192). 

In status epilepticus (i vide p. 507) the temperature usually 
rises considerably. Increased heat production may be said 
to be due also to disturbance of the heat-regulating mechan¬ 
ism of the brain, by which the heat loss is not in proportion 
to the heat production. Moreover, I have found, as Hill, 
Craig and Turner have described, that in general paralysis 
the arterial pressure, as measured by Hill and Barnard’s 
sphygmometer, is high—usually considerably higher than 
one would expect on feeling the pulse or listening to the heart 
sounds. I have met with it as high as 200, the normal being 
120. The subjoined table illustrates some of the points:— 

It will be observed that the pressure is usually above 
normal, except in the third stage, when it may fall consider¬ 
ably below normal. It was also observed in some cases that 
after a succession of seizures of a severe nature, lasting 
some time, the pressure fell, but rose again on recovery 
from seizures. 

The cases are not numerous enough to make any very 
definite statement, except that in the first and second stages 

No. Initials. Sex. Natu 


of the disease the arterial pressure is invariably higher than 
normal, and that further observations which I am making 
will probably confirm the opinion that, after a succession of 
seizures, the arterial pressure falls, owing to cardiac failure ; 
possibly also cholin escaping into the circulation may dilate 
the vessels of the splanchnic area. 

The pressure was taken in five cases of the juvenile form 
of the disease, and was found to be higher than normal, 
especially in relation to the character of the heart sounds, 
which were usually feeble. 

It will be observed that, as a general rule, the arterial 
pressure rises during the seizures, and this increase of pres¬ 
sure may be explained in several ways :— 

(1) Vaso-motor irritation .—One of the most constant, 
probably the most constant, macroscopic change found post 
mortem is a granular condition of the floor of the 4th ven¬ 
tricle. It is here that physiologists place the vaso-motor 
centre. Neuroglia proliferation probably is associated with 
irritation and formative processes; we might, therefore, 
consider it possible that there is a continuous vaso-motor 
excitation, and this would cause spasm of the arteries and 
increased arterial pressure. As a rule, however, we do not 
find cardiac hypertrophy; at least, not a hypertrophy at all 
comparable to chronic Bright’s disease. Yet we have seen 
that the arterial pressure is as high, or even in a few cases 
much higher in general paralysis ; but it must be remem¬ 
bered that chronic Bright’s disease is a slow process which 
gradually leads to cardiac hypertrophy, whereas general 
paralysis is an acute process which rarely lasts more than 
two or three years. 

(2) Auto-intoxication, or altered conditions of the blood, 
might be assumed to account for the high arterial pressure ; 
this, so far as Professor Halliburton’s and my experiments 
upon cholin and neurin go, will in no way account for this ; 
in fact, cholin, which is a weak cardiac muscle poison, 
causes lowering of the blood pressure mainly by its dilating 
effects upon the splanchnic area; and we could find no 
other toxic product in the cerebro-spinal fluid which, when 
injected into the veins of animals, produced any effect upon 




the arterial pressure. Moreover, a solution of the alcoholic 
extract of the blood of two cases of general paralysis taken 
by venesection during seizures produced this same effect 
as cholin; consequently we cannot suppose that the cholin, 
after it has escaped into the blood, is converted into the 
allied body neurin, a most powerful poison, which, although 
producing a primary fall of blood-pressure, produces after¬ 
wards a marked rise of arterial pressure. We must there¬ 
fore assume that the rise of blood pressure is not due to 
auto-intoxication from disintegrating brain tissue; it is 
possible, however, that profound modifications in the 
cerebro-spinal fluid, as evidenced by the presence of con¬ 
siderable quantities of nucleo-proteid and cholin (constituents 
not existing in the normal fluid), might set up irritation 
and formative proliferation in the ventricles of the brain 
where the fluid is most abundant, thus accounting for the 
glia cell-proliferation and irritation of the vaso-motor centre. 1 

After a considerable number of convulsions, the pressure 
falls to even below that of the normal, and if the patient 
dies it may be assumed that there is heart failure. Exam¬ 
ination of the muscle substance of the heart, as we shall 
see, explains why heart failure should arise. In the 
epileptiform seizures, if general and severe, we have a con¬ 
dition more or less of asphyxia arising as in Cases pp. 199-202. 
Of course, the increasing venosity of the blood, the spasm 
of the muscles, the accumulation of imperfectly oxidised 
fatigue products in the blood, together with possibly the 
escape into the blood of toxic substances such as cholin, 
arising from the disintegration of nervous tissue, will collec¬ 
tively embarrass the heart by the increased work which it 
has to do to overcome the peripheral resistance, especially 
when it is supplied with imperfectly oxygenated blood 
containing toxic substances. 

The result will be dilatation of the right side of the 
heart and engorgement of the venous system ; but this we 
shall see, in discussing the subject of status epilepticus, 

1 Binawanger considers that changes in the cerebro spinal fluid caused by 
accumulation of the products of destruction of the decaying nervous structures 
produce secondary changes in the pia and in the ependyma of the ventricles. 
Progressive Allgemeine Paralyse , von. Prof. Krafft-Ebing, p. 72. 


acts back upon the brain, increasing the excitability of the 
discharging nervous centres, and producing either their 
exhaustion or death; the fatal termination being due, in a 
number of these cases, to heart failure, the muscle substance, 
as we shall show, being in a state of acute fatty degeneration. 

Examination of the heart and striated muscles .—The 
fact that many people die in general paralysis with naked- 
eye appearances of normal heart and lungs led me to examine 
systematically the heart muscle and striated muscles of the 
diaphragm and pectoralis major muscle in a large series of 
cases of patients dying at Claybury. Fatty degeneration of 
the heart has been described by previous workers; Dr. 
Mickle mentions it in his text-book, and Dr. Campbell 1 has 
described it and associated this condition of the heart with 
degeneration of the vagus nerve and the fatty changes in 
striped muscles to changes in the motor-end plates. 

I have examined five or six cases of diphtheritic paralysis 
in which there was extensive fatty degeneration of the heart, 
but in only two of these cases could I find any evidences of 
a nerve degeneration. The question arises whether this 
degeneration in general paraylsis is due to auto-intoxication. 
I have examined 112 cases successively, of which seventy- 
five were general paralytics. Of these, fifty-three (about 70 
per cent.) showed some signs of fatty degeneration in one 
or more of the muscles examined ; out of the fifty-three, 
six were very fatty, thirteen markedly fatty, and thirty-four 
fatty in a slight and variable degree. As so many of these 
people die with bedsores, gangrene of the lungs, broncho¬ 
pneumonia, ulcerative colitis, cystitis and other forms 
of terminal septic infection, I thought it would be well 
to satisfy myself that the fatty change was not due to 
this cause. I therefore asked Dr. White, late assistant 
medical officer at Claybury, to help me in making a sys¬ 
tematic bacteriological examination of the blood in the great 
longitudinal sinus, and also from the cerebro-spinal fluid of 
a series of cases. The cases were not selected, but taken as 
a matter of routine in the course of post-mortem examina- 

•A Contribution to the Morbid Anatomy and Pathology of the Neuro¬ 
muscular Changes in General Paralysis of the Insane, by Alfred W. Campbell 
(The Joui'nal of Mental Science , 1894, April). 



tion. Eighty-three cases were examined. Organisms of 
various kinds were isolated in eighteen cases ; these organ¬ 
isms varied in a remarkable degree, and it was not found 
that any organism occurred with any constancy in any par¬ 
ticular class of case. Before September, 1896, the cadavers 
were simply placed in the mortuary at the ordinary tem¬ 
perature of the air to await the autopsy. Since then the 
cold chamber has been working, and it is the custom to 
place the body as soon after death as possible in this room, 
where it is kept at a temperature of 32° F. The number of 
cases from which micro-organisms could be grown materially 
diminished after this. I have not, therefore, been able to 
associate the fatty degeneration with micro-organisms. At 
first, owing to the fact that the notes in the case book did 
not record seizures in some of the cases, I was not led to 
associate the fatty degeneration I found with this condition; 
examination, however, of the muscles and heart of epileptics 
who had died in status exhibited the same acute fatty 
change; therefore, I was led to make more careful inquiries 
about the conditions antecedent to death, and I have found, 
as a rule, that marked fatty changes have occurred only 
in those cases which have had seizures. Seeing that 
so excellent an observer as Dr. Campbell had described 
degeneration of the vagus and changes in the motor end- 
plates of the striped muscles, I made a systematic examina¬ 
tion, both by sections of the nerves and by dissociation, 
staining with osmic acid and Marchi fluid, but I have failed 
to find any degeneration of the nerves which would account 
for the fatty degeneration. Dr. Campbell has figured a 
transection of a bundle of the vagus nerve stained by 
Weigert method, in which only a few large medullated 
fibres are seen; but normal sections of this nerve, stained by 
this method, will show some bundles having this appearance, 
whereas if the nerve is placed in Marchi fluid and cut in 
transverse section, it will be seen that between the coarse 
myelinated fibres are immense numbers of fine medullated 
and sympathetic fibres which are unstained by the hsema- 
toxylon. Dr. Barratt has prosecuted this research further, 
and his results entirely coincide with my own. The accom- 


panving i/iiutoujicrogcapti of a vagus nerve was fjdtm a caw of 
general paralysis with extreme fatty (k'-gboeratitm of the heart. 

With regard to theChange:-; in the iuotor end plates, X 
know of no siifficiehtly telfftble method by Which any com- 
pai-aiive results between the mmmil and •d.iseiLse.X conditions 
could be obtained; I find it very v4MpicavJt m show • ihv*<r 
structures iu normal human maafclei That there maybei 
poisoning of the motor end plates and of ;peryd 

fibres I think is tjuitp possihle ; but I fmvii sblihnjK hiufid 
marked changes iu the peripheral nerves/ Fre<pteuUv in. 

Pb^tomlcr^riipb of transverse s&z&iii : uf Yagur^m- stain-ad- Uv M.arclii 

■ •* a _. . r '• ■■■'-- t . 1 i‘: ' • •’ < i v • ■ • v ■' : v -» »Y'v * ' -j ■■ ■ ’ . .. . ■’ 

fluid from n oft*ie nf '.general paralysis wlfc& Vary matkod iaiiy 4^aii&t>vtum of 
the heart. Tlie scattered coarse- myc-liitatel lifoies* afB iVitt*rmiXjQt.I v»/iE,L» 
the much ui-re swin*rous fine fibres* M&gnifiaatiou UbiX 

general paralysis symmetrical bultai appear oil the body in. 
situations whore pressure effects could not operate,mid upon 
examination of otic degenera¬ 
tive changes iu the tw'iga nf the cut&nypUe to 

these skin areas, also ehromolytio changes in the posterior 
spinal ganglia {tride- tigs. .1 and 2, p. ',Y2 ( .i, and plate v., jig. 2). 



Method of examination of the muscles. —Small pieces 
of the heart, the diaphragm, and pectoralis, sometimes the 
thumb muscles, about the size of a clove, were taken and 
placed in Flemming’s solution or in Marchi fluid; they were 
allowed to remain there a few days, then thoroughly washed, 
the fibres dissociated with needles and mounted in Farrant’s 
solution. A large number of the specimens, especially those 
cases in which the results of dissociation were unsatisfactory 
or doubtful, were embedded in celloidin, and cut in sections. 

Results of microscopical examination of this large 
number of cases have led me to the following conclusion :— 

(1) In patients who die from intercurrent complications 
during the first or second stages of the disease, but without 
previous prolonged epileptiform seizures, the muscles and 
heart show, as a rule, normal striation. There may be some 
few fibres with a few very fine black dots indicating fat 

(2) In patients who escape complications in the first and 
second stages, and pass on into the end of the third terminal, 
emaciated asthenic stage, dying from exhaustion, with or 
without terminal infection from gangrene of lungs, cystitis, 
bed sores, &c., the fibres are opaque, attenuated, striae 
indistinct or even lost, and all the appearances of brown 
pigmentation of the heart, but as a rule unless they have had 
seizures no evidence of black osmic acid stained fat granules. 

(3) In patients who die after a succession of seizures, and 
practically in proportion to the length and severity of the 
same, one finds fatty degeneration, e.g.. Cases G. M., p. 199, 
E. C., p. 202, A. R., p. 282, are typical examples. The fat 
is deposited in very fine globules through the substance of 
the fibre, usually the case is too acute for it to obscure 
entirely the striation, so that the minute globules have run 
together, but in the case of E. C. this was so in the fibres 
of the musculi papillares of the heart. Usually the heart is 
more affected than the striped muscle, and the fibres are 
more generally affected. In the striped muscle one sees the 
globules of fat usually of uniform size arranged in parallel 
rows between the fibrils as is described on p. 504 in Status 
Epilepticus. They are probably in the sarcoplasm of the 


(4) The fatty change in muscle cannot, as a rule, be 
recognised by the naked eye appearance. 

(5) In the connective tissue around the muscle fibres 
phagocytes containing fat were often present. 

(6) I consider that this fatty change is of importance in 
showing imperfect metabolism, and it is indirect evidence of 
auto-intoxication. This subject is discussed more fully under 
Status Epilepticus, p. 502, for the change is exactly the same, 
and in all probability caused by the same conditions. 

The following case (one of four that I have seen) illus¬ 
trates the effects of thrombosis of the great veins opening 
into the longitudinal sinus, causing epileptiform convulsions 
and hyperpyrexia, acute fatty degeneration of muscles, liver, 
kidney, &c. 

G. M., grocer, married, admitted to Colney Hatch, August 10, 1898. 
Not previously under care or treatment. Duration of existing attack a 
few days. Supposed cause, worry and overwork. No insanity or epilepsy 
or neuropathic family history. Wife states that on May 1 he had two 
fits for the first time in his life, and he had two more fits a month ago. 
He never had fits at any other time. He only became wrong in his 
mind after the latter two fits. During the fits he lost consciousness, was 
convulsed and black in the face, and they lasted two or more hours. 
Never saw him drunk; drinks only moderately. He did not lose power 
after the fits. Some years ago before marriage he was gay. Father said 
that he had venereal disease six or seven years ago. He has no children. 
He had a semi-imbecile expression. He spoke in a hesitant, drawling 
manner. He had no knowledge of time or place. There was slight 
paresis of left side of face, and he was apathetic and depressed. He com¬ 
plained of no headache and he had no vomiting.—C. B. Gervis. 

On August 17 I was taken by Dr. Gerv is to see the case. I ascertained 
that from 8.45 p.m. till 8 p.m. the previous day he had had twenty-one 
fits, through the night the same number, and he has had eight since six 
o’clock—fifty in all. The attendant states that the fits start by conjugate 
deviation of head and eyes to the left, and the mouth is drawn to the left, 
then the left arm, left leg, and then right leg are convulsed. Unconscious 
the whole time. Fits last seven or eight minutes. He is now lying on his 
back quite unconscious, breathing stertorously. The left eye is closed, 
the right half open, the right eye turned inwards, the left outwards. 
Pupils medium size, equal, no reaction to light, conjunctival reflex absent. 
Knee-jerks present on right side, absent on left. The face shows no 
paralysis, as the cheeks are not blown out. He is now twitching in the 
left nostril. The limbs are flexed and there is no rigidity. The left arm 
is flexed at elbow, flexed at wrist midway between pronation and supina¬ 
tion, the thumb and fingers flexed at metacarpo-ph. joints. The left foot 
extended and inverted ; both legs are extended. 



A little later both eyes were open, and still conjugate deviation of the 
eyes, but not of the head, was observed. I saw him just at the end of a 
fit. During the fit there was conjugate deviation of the head and eyes, 
and clonic spasms in the left arm, but none of the leg. Temperature 
108*2°. No cardiac affection. Syphilis six years ago. Scar on penis, 
scar on right groin. Pulse small and weak. When Dr. Gervis saw him 
yesterday the fits were on the right side, with conjugate deviation to the 
right. Previously there w r as ankle clonus and exaggerated knee-jerk on 
the right side. 12.15 p.m.—Fit observed by myself. It started with 
flexion of wrist and metacarpo-ph. joints, five minutes later the arm 
convulsion ceased and twitching of left side of face occurred. There was 
not a definite march to the fit now*. The temperature went up to 107° at 
six o’clock, and the fits continued till death at 6.50 p.m. 

Autopsy (fifteen hours after death)—No signs of putrefaction; no 
bruises or scars. Rigor mortis w r ell marked. Body well nourished. 
Heart —Weight, oz., flabby and greasy, no valve lesion. A portion 

taken in Miiller’s fluid. Lungs —Healthy, oedema at bases. Right, 
22£ oz.; left, 19£ oz. Aorta commencing atheroma all the w r ay down, 
especially about orifices of vessels. Liver —40 oz., no scars, fairly 
normal, rather greasy. Piece taken in Miiller’s fluid. Kidneys —Right, 
8$ oz.; left, 4 oz. Capsule strips, no scars, pale and flabby, greasy, and 
probably early fatty change. Portion taken in Miiller’s fluid. Spleen — 
8 oz. Small, thickening of capsule about the size of a pea. Cranial 
cavity —Skull cap normal. Veins of dura and longitudinal sinus con¬ 
gested, filled with dark clot. On removal of dura mater the membranes 
appear congested. Pia arachnoid very red, not opalescent; convolutions 
not atrophied, rather flat, indicating increased intracranial pressure. 
Brain weight, 52^ oz. Arteries appear normal; no evidence of syphilitic 
growrth or basic meningitis. The veins upon the surface of the brain, 
especially about the central convolutions, very congested, and appear 
filled with a firm clot, which cannot be drawn out. Very little fluid in 
ventricles. The brain is well formed, and the convolutions appear par¬ 
ticularly well formed and regular as regards topography. The ascending 
frontal and parietal and frontal convolutions are quite easily distinguished. 
The membranes are adherent over the first frontal on both sides, but 
there is no agglutination of the tw f o hemispheres in front. The lateral 
ventricles are not dilated, but are slightly granular. There is apparently 
no excess of fluid. The middle cerebrals were removed, but to the naked 
eye they, together with basilar and vertebral arteries, appeared quite 
normal. The brain is soft and w r atery, 4th ventricle slightly granular; 
whereas the hemispheres are extremely congested and puncta cruenta 
very obvious in the white matter, the pons appears paler and softer than 
natural. Portions of the right paracentral lobule taken in Miiller, in 
spirit, and in 2 per oent. formol. Portions of the base of 1st frontal, ascend¬ 
ing frontal and parietal in Miiller, also pons, medulla, and cerebellum. On 
slicing the hemispheres it was noted that the left hemisphere in the 
frontal region w r as extremely soft and dotted all over wdth little dark 
points, congested veins, possibly haemorrhages. This, however, w'as not 
so obvious as in the frontal and central portions of the right hemisphere. 


Here the white matter in particular, but the grey matter of the cortex 
also to some extent, presented an appearance resembling early red 
softening. Areas the size of a shilling or a half-crown were observed in 
various situations softened and dotted all over with little dark haemor¬ 
rhagic puncta, especially in the distribution of the vein which was filled 
with the adherent clot. There was not much cerebro-spinal fluid to be 
obtained, and it was not kept, as it was so stained with blood as to 
be practically useless. 

August 22.—Examination of the heart, diaphragm, pectoral and 
extensor com. digit, of left arm, after staining in Marchi fluid and teasing 
up the fibres and subsequently mounting in Farrant’s solution. The 
heart muscle showed very extensive fatty degeneration. The diaphragm 
showed about 1 in 10 fibres with early fatty degeneration, and the other 
two muscles showed here and there a fibre with fine dust-like particles 
scattered through it. 

Subsequently sections were made and extremely well-marked fatty 
degeneration was observed in the heart muscle. Also some degeneration 
in the diaphragm and other muscles. The liver showed very marked 
fatty degeneration, and the kidneys also, especially the first convoluted 
tubules were stained black by osmic acid; possibly some of this fat may 
have been picked out by the epithelium from the blood. 

Sections of the ascending frontal and paHetal .—The upper part, 
including the large anastomotic vein, were examined after staining by 
the following methods: Nissl, Weigert iron, Marchi and Marchi-Pal, 
also by Held's method and dahlia carmine. They show the following 
characters: The large anastomotic vein is blocked on both sides by an 
organising thrombus. The wall of the vein and the clot is infiltrated with 
leucocytes, most of which are small and stained deeply with basophil 
dyes (vide photomicrograph, page 2Q3). The pia arachnoid membrane and 
the perivascular lymph spaces show enormous numbers of leucocytes 
similarly stained. The small veins are gorged with blood and the 
surrounding lymphatic spaces are dilated, so also are the spaces in which 
the cells lie. None of the cells show the normal granules of Nissl, either 
in the body of the cell or on the dendrons. They are stained throughout 
a dull purple colour (when a double stain, c.y., polychrome methyl, blue, 
is used). Whether this is due to the high temperature or the changes 
incidental to death of the nerve cells I am unable to say. Probably the 
convulsions are the expression of the increased irritability of the nervous 
structures prior to death. Instead of the normal granules of Nissl, the 
cells examined with an oil immersion are seen to owe their diffuse stain 
to a fine-coloured dust scattered through the body of the cell (vide 
plate viii., fig. 4). The nucleolus alone is stained deeply. The appear¬ 
ance of the cells is very similar to that observed in animals which have 
died in convulsions after ligation of the arteries. The great dilatation 
of the perivascular and perineuronal spaces is similar to that observed in 
animals after ligation of arteries in which there was enormous venous 
engorgement and congestive stasis. By the Marchi method a number of 
degenerated fibres of large size are seen in the motor area and the pyramids 
of the medulla show a large number of degenerated fibres on both sides. 



The nerve cells, from which these degenerated fibres spring, must have 
been attacked at least six days prior to death. Probably they represent 
the degeneration resulting from the seizure a month before admission. 
Numbers of the leucocytes in the thrombus and in the wall of the 
thrombosed \ein are filled with black particles, showing that they have 
taken up the fat from the degenerated nervous tissue. 

Examination of the ascending frontal and ascending parietal convolu¬ 
tions by the Marchi-Pal method shows an almost complete disappearance 
of the tangential system of fibres. 

E. C., aged 87, admitted to Claybury Asylum in the early stage of 
general paralysis. The patient was a man of very fine physique and of 
handsome features. He had been a medical student, unqualified 
assistant, secretary and various other occupations until finally he had 
sunk to time-keeper on the tramway. He had led a rackety life, had 
indulged in alcohol, and had had syphilis eighteen years ago, hard sore, 
sore throat, eruption and severe headache, from which he obtained relief 
by mercury. Eight years later he suffered with diplopia. He has been 
married twice; first wife no children; second wife one child, alive and 
healthy. The mental affection commenced with a fit in the night twelve 
months ago, it was followed by delusions of wealth and grandeur. 

Physical condition. —Well-nourished and physically strong. Palmar 
psoriasis. Pupils small, unequal, irregular and inactive to light, but 
react to accommodation. Speech slightly slurred and hesitant. Knee- 
jerks present, slightly exaggerated. Slight tremor of face muscles and 

Mental condition .—He has a fair knowledge of time and place, and 
can give a good account of his past history; he shows very little de¬ 
mentia or loss of memory. His condition improved so much that his 
friends, being anxious to take him, he was put down for discharge. He 
then had a succession of epileptiform seizures, which were followed by 
mental and physical impairment. Each series of fits that he had 
left his verbal and written speech more impaired, although a few 
days after the fits had occurred a certain amount of recovery 
would take place, showing that the effect was partially due to func¬ 
tional (probably vascular) disturbance. The curious condition of verbal 
amnesia and verbigeration he showed after the fits is illustrated 
as follows :—Shown a key and asked, What is this ? He would spell the 
word K-E-Y, Key. When shown a coin, a pencil, or any other common 
object he would persistently repeat K-E-Y, Key. Asked to read the 
newspaper—he read Sandown Races, and this seemed to recall the w-ord 
Chadwick. Every object that was shown him afterwards was Chadwick. 
A book was a place called Chadwick. A key is now* a place called 
Chadwick. When, however, told it was a key, he repeats key, but the 
next instant reverts to a place called Chadwick. Asked his wife's name, 
he replied Alice, and now in reply to all questions he mixes up Alice with 
a place called Chadwick. Yet at times he seemed to be conscious that 
what he had said was incorrect and meaningless. A few days later this 
curious condition had passed off. There was no paralysis, but some 


wuidiherfs inth^nght hiked 4b compared with the left- fj^n^lliory wda 
fairly good fttJtl thcw nothing noticeable ftr the except, 

hesibmcy and slight. tremdiux 

July* 189?.—He h&d another aerie* of titsjuid; thecondition of 
^peeeb$ecmTe^^ fits, When be wtys rip* I asked jhm to write 

name and bow tong' he. had been here. He vmit<; v 14 f ha ving been 
•fctotog .-beening here teen her* thirteen [xz&x and fbxSee moth/ 1 ' frit 
September? 1897r be bad « very xiwm : $»i vpitepittbim fits, 

idloetmg ©specially the right able ^ he bex&m£ ^ita Wct>i^fei6ri^, and 
four d>iys after the onset of the fits, he diem in.& state of asphyxia. 

;morfe4.-^5eiieral venous i^igovgemeht with itohtimjrijr dfc 
tended nght heart. The .brain-v'hc^d ^eat congestion of tjic veins, pia 
•ai^cftxioid thickening over- the whine of the .-frontal central and parietal 
convolutions- with adhe^ione, ^omowbitt dilated. ventricles- haymg a 
g^mdsu: condition of tic ^petulv^na. ' 0 - / 

Afiorn^roph'n./ erwrr7/G/f>( l h»?r.--The brain showed disappearance of the 

ii'iu^entiai fibres of. Brocay* corn-olutioa and of the Central convoluticiris. 
Nlsrf method pybEhted degenerative change* in the cortical cell 6, pro¬ 
liferation of glia cells, and marked cellular pjnthferatimt in the pemas- 
cubtr lymphatics. There was marked degeneration of '.the pyramidal 
system* of .fibvos in the ehpeule, po?w, medulla and spinal .cord' 

eidnhited% aii^ciu'-hifcfhod^ rv)|^'K.v\. V ' ;-' 

Examination of the heart* striated muscles* liver and kidneys showed 
by Marehi m^nfc acute fatty dcgencrution. 

The tuiismjli papilkres of the heart exhibited very marked change, 
tW fM* {.wtldh^ \S^rb of ywous siaea, and; the- -^breftAwere *atahfed[ 
mtehaeiy tfek ht the cmnu? acid. Examination of' t.ha vagus ttfervea 
4v Or* Jiorrat t ry the Marchz method* 

Section of portion of great axmfctcanatic vein, ^bowing lh/uen pilled with 
organising- tlirombus, and wall infiltrated with leucocytes? |v; ML 



I undertook the following investigation at the sug¬ 
gestion of Dr. Mott, who wished to know whether the 
blood of patients suffering from general paralysis of the 
insane differed in any marked degree from that of people 
free from this disease. The patients whose blood was thus 
examined were selected cases undergoing treatment in the 
Claybury asylum. 

The blood in almost every case was obtained by puncture 
of the ear of the patient, the skin of the ear having been 
previously rendered aseptic by thorough cleansing followed 
by application of antiseptics. 

The blood in each case was examined so as to 
ascertain :— 

(1) The percentage of haemoglobin. 

(2) The actual number of red and white corpuscles 

(3) The relative proportion of red to white corpuscles. 

(4; The relative proportions of the varieties of leucocytes 

to one another. 

Methods Employed. 

I. The Estimation of the Number of Leucocytes. 

The instrument used for this purpose was that known as 
the “ Thoma-ZeiBS hseinacytometer.” The method of count¬ 
ing the blood-corpuscles by means of this instrument has 
two great advantages over Gower’s haemacytometer, viz.: 

(1) It is more accurate. 



Each leucocyte previous to being counted has been 
stained a deep blue colour. Consequently it is quite easy 
to distinguish the leucocytes from the red corpuscles and 
to rapidly count the number of leucocytes present within 
the field of the microscope. 

(2) It is easier to use. 

The blood is only diluted to the strength of 1 in 10 
when counting the leucocytes, consequently one can get 
a considerable number of white corpuscles within the field 
of the microscope. 

II. The Classification of the Leucocytes. 

The leucocytes were first stained with Boehmer’s haema- 
toxylin followed by eosin. The basis of the method of 
classification adopted consisted in observing 500 leucocytes 
successively in each case and then noting the size, shape 
and number of the nuclei present in each leucocyte, to¬ 
gether with the relative bulk of the nuclear substance, to 
the remainder of the cell substance of each leucocyte. 

III. The Estimation of the Haemoglobin. 

This was done by means of Oliver’s baemoglobinometer. 
A known quantity of blood is diluted with water and then 
the colour of the resulting solution of haemoglobin is com¬ 
pared with the colours of a number of carefully prepared 
coloured slabs, candle-light being the means of illumination. 

Each coloured slab corresponds to a definite percentage 
of haemoglobin. By means of small coloured glass slabs 
great nicety can be arrived at in matching the colours. 

This method is easy to use and takes little time. It 
has one great advantage over Fleischl’s method. This is 
that the colour of the different slabs exactly corresponds 
with that of blood diluted with various quantities of water 
and observed by candle-light. 

Also by the use of the coloured slabs of glass the per¬ 
centage of colouring matter in the blood can be measured 
with much greater precision by Oliver’s instrument than 
by that of Eleischl. This is particularly the case when 
examining blood containing an abnormally small percentage 
of haemoglobin. 



Research Scholar in Neuropathology to the London County Council. 

The central nervous system is rich in phosphorus-con¬ 
taining substances, some of which are present in the form of 
phosphorised fatty material (protagon, lecithin). In nerve 
degeneration this latter splits up into compounds of simpler 
constitution, as is indicated by the separation of fatty 
material, revealed by osmic acid staining, to be again at 
a later period absorbed or removed. The course taken by 
the phosphorus-holding substances liberated at the same 
time appears to have received scant attention. In order to 
throw some light upon this point, it was determined, at the 
suggestion and with the assistance of Dr. Mott, to estimate 
the amount of phosphorus present in the cerebral hemi¬ 
spheres and spinal cord in conditions in which degenerative 
changes might be expected, in particular in cases of general 
paralysis of the insane where wasting of nervous tissue 
takes place. It was necessary to examine also perfectly 
healthy material for comparison, and for this purpose the 
hemisphere and cord in cases of death from accident were 
selected, but, owing to the difficulty of obtaining perfectly 
healthy material, up to the present only one such normal 
hemisphere and cord have been examined. 

The whole of one cerebral hemisphere, usually the left, 
together with the corresponding half of the corpus callosum 
but not including the corresponding basal ganglia, which 
were carefully dissected out, was taken for the estimation of 
water and phosphorus in the various cases examined. No 



attempt was made to remove the pia arachnoid and all 
manipulation of the tissue was avoided, the hemisphere 
being simply cut up into slices of 1 to 1£ centimetres thick 
and transferred without any delay to glass dishes for drying. 
It was thought preferable to leave the pia arachnoid attached, 
because of the difficulty of removing this membrane without 
in some cases at the same time tearing away portions of the 
grey matter, while during the whole of the time occupied by 
this procedure evaporation of water and draining of serous 
fluid is occurring to an extent which would probably vary 
in different cases and thus affect the subsequent analysis. 
No attempt was made to separate grey and white matter, 
principally because of the difficulty on the one hand of com¬ 
plete separation and on the other hand of selecting in 
successive experiments exactly similar areas of grey and 
white matter. For a similar reason no attempt was made 
to submit any of the various regions of the cerebral cortex 
to analysis. 

In dealing with the spinal cord, the dura mater and 
arachnoid were removed and the nerve-roots divided at 
their superficial origin with as little delay as possible 
before weighing and drying. 

As the estimation of phosphorus in organic material is 
tedious and somewhat complicated, being, moreover, fertile 
in sources of error, it will be well to describe now the 
analytical method adopted in this research. 

The Estimation of Water and Phosphorus. 

The nervous tissue to be examined, after removal from 
the body, was weighed and placed with the least possible 
delay upon Petri dishes in a drying-oven kept constantly 
at 100’ C. At this temperature drying takes place rapidly, 
but a slight degree of charring is noticeable and the tissue 
becomes brittle. A certain amount of slightly turbid, faintly 
yellow fluid, it was noted, separated from the tissue after 
being some hours in the drying-oven, and at the end of 
twenty-four hours the exposed surface of tissue became con¬ 
verted into a brown parchment-like layer and evaporation 



proceeds slowly. The tissue must now be turned over and 
its position in the glass dish changed from day to day until 
at the end of from three to five days it is sufficiently hard to 
be cut up into small pieces with a clean pair of scissors. 
These pieces are then collected in a weighing-bottle, which 
is kept in the hot-air bath until the daily decrease in weight 
becomes less than *5 per cent, of the whole, and then trans¬ 
ferred to a sulphuric acid desiccator, where drying is com¬ 
pleted in vacuo at the temperature of the room, the sulphuric 
acid being repeatedly renewed. The nervous material 
adhering to the Petri dishes is as far as possible scraped 
away and transferred to the weighing-bottle and the weight 
of the remainder determined and added to that of the dry 
material in the weighing-bottle. The nervous tissue when 
dried is of a brown tint and has a waxy aspect. It is hard 
and readily cut or broken up, but cannot be reduced to 
a powdered state. The time occupied in drying a hemi¬ 
sphere at 100° C. was about four weeks. 

Instead of drying at 100° C., the nervous tissue may be 
put into a hot air bath at 60° C., or it may be dried in vacuo 
over sulphuric acid at 0° C. In the former case the tissue 
does not become charred, is less dark in colour, and much 
less brittle, but the time occupied in drying is increased ; in 
the latter case the tissue is of a pinkish-white waxy aspect, 
almost free from any brownish tint, and the time occupied 
in drying is more than trebled, while if the temperature 
occasionally rises colonies of micro-organisms may appear on 
the surface. At 100° C. about 15 per cent, more water is 
given off during drying than at 0° C. 

The whole of the dried material thus obtained is next 
thrown in small quantities at a time into a nickel crucible 
containing in the melted state a mixture of caustic alkali 
and potassium nitrate, when the whole of the organic matter 
is destroyed, and the phosphorus present becomes converted 
into sodium orthophosphate. The most convenient mixture 
to work with is that recommended by Gutnikov, 1 namely, 
three parts of caustic soda to one part of potassium nitrate; 

1 “ Zur Lehre von der chemisohen Zusammensetzung des menschlichen 
Gehirns,” Zeitschr. f. Psychiatric, liii., 270-379, 1896. 




and of this mixture ten parts are to be used for one part of 
dried organic matter. Care must be taken to obtain caustic 
soda which is free from phosphate, and should water be 
present this must be driven off by heat until all spitting has 
ceased, when the fused mass should be poured into a second 
nickel crucible and the organic matter added. If the fused 
mass has too high a temperature the dried nervous tissue 
when thrown in takes fire, and considerable frothing occurs. 
If on the other hand the fused mass is insufficiently hot, the 
dried nervous tissue is merely coated by a white crust of 
solidified alkali, and no further reaction ensues. When, 
however, the proper temperature is obtained, the organic 
material is rapidly destroyed at a heat below redness and the 
destruction proceeds regularly without flame or frothing. 
There is no need to heat the crucible from below during the 
process, sufficient heat being given out to maintain the 
temperature of the whole. A slight degree of spitting 
generally occurs, especially towards the end; to avoid loss 
from this cause, the crucible should be covered with wire 
gauze. An abundant discharge of gas occurs during des¬ 
truction, and a small amount of caustic soda is carried away 
by the gases given off, which are at first colourless but rapidly 
assume a dense white aspect as they become cooled, and 
condense on glass with an alkaline reaction, and are very 
irritating when inhaled. 

After cooling, the fused mass, which contains all the 
phosphorus present in the form of sodium ortho-phosphate, 
is dissolved in water and nitric acid added until no further 
C0 2 is liberated. This is best carried out in a flask or 
similar vessel, so as to avoid loss by the fine spray given 
off during effervescence. The liquid is then warmed to 
drive off carbon dioxide, filtered and mixed in the requisite 
proportions with a solution of molybdate of ammonium 
rendered acid with nitric acid. 1 After standing for twenty- 
four hours some of the supernatant liquid is tested with 
molybdate solution for phosphoric acid, and if precipitation 

1 This has the composition : ammonium molybdate, 60 grs.; ammonia solu¬ 
tion (specific gravity 960 = 10 per cent.), 400 c.c.; water, 400 c.c.; nitric acid, 
500 c.c. Of this 5 c.c. are required to precipitate *001 gr. P. 



is complete the precipitated phospo-molybdate of ammonium 
is collected on a filter-paper and then dissolved in strong 
ammonia. The solution thus obtained is filtered and pre¬ 
cipitated with the requisite amount of magnesia mixture, 1 
when the phosphoric acid present is converted into triple 
phosphate, the precipitate, however, containing a certain 
amount of molybdic acid. At the end of twenty-four hours 
this precipitate is collected on a filter-paper, washed with 
dilute ammonia and then dissolved in as small a quantity of 
hydrochloric acid as possible. The filtrate from the triple 
phosphate precipitate should be tested for phosphoric acid 
to make sure that precipitation is complete, and to the 
solution of the precipitate in dilute hydrochloric acid 
sulphuretted hydrogen is added to convert the molybdic 
acid present into sulphide of molybdenum, which falls as a 
brownish-black precipitate, the liquid first turning blue, 
unless molybdenum is present in exceedingly small traces, 
when only a brown discolouration occurs. The precipitation 
of molybdenum sulphide is tedious, sulphuretted hydrogen 
sometimes requiring to be repeatedly passed through the 
solution ; the precipitation is aided by heating. 

As soon as the precipitation of molybdenum is complete, 
the ammonia is added to the filtered solution, when 
ammonio-magnesic phosphate is again thrown down. After 
standing twenty-four hours this is collected on a filter-paper 
of known ash and dried. The precipitate is then heated in 
a porcelain crucible to a bright yellow heat, when it is con¬ 
verted into magnesium pyrophosphate, which exhibits at 
this temperature a curious deflagration, due to the passage 
of the compound into a different physical state. The filter- 
paper is incinerated separately in a coil of platinum wire. 
As triple phosphate is slightly soluble in a solution of 
ammonia and ammonium chloride,* it is necessary, especially 

1 Crystals of magnesium sulphate, 1 part; ammonium chloride, 2 parts; 
water, 8 parts; solution of ammonia, 4 parts. Of this solution 10 c.c. will 
precipitate -1 gr. P. 

2 1,000 grm. of a mixture of 3 parts of water and 1 of ammonia solu¬ 
tion dissolve only a quantity of triple phosphate corresponding to *004 grm. 
magnesium pyrophosphate. If 18 grm. of ammonium chloride are present, 
a quantity equal to *011 grm. magnesium pyrophosphate is dissolved 



when the quantities dealt with are small, to add to the 
weight of pyrophosphate of magnesium collected a small 
correction representing the amount present in the filtrates 
from the triple phosphate precipitate. The correction 
usually amounted to about 2 per cent, of the whole in the 
case of the spinal cord, but is much smaller when a whole 
hemisphere is submitted to analysis, being then less than 
5 per cent, of the whole amount of magnesic pyrophosphate 

Pathological Examination of the Cerebral Hemi¬ 
spheres and Spinal Cords. 

The percentage of water and phosphorus in the cerebral 
hemisphere was determined in nine cases [Table I.]. In 
all except the last the hemisphere selected was the left. 

The five cases of general paralysis of the insane chosen 
were typical cases of this affection; that is to say, the 
clinical course of the affection was characteristic, and at the 
post-mortem the cerebral convolutions were found to be 
wasted, the pia arachnoid was opaque and thickened over 
the vertex and its meshes distended with clear yellow fluid, 
the ventricles being also distended with fluid, and the epen¬ 
dyma of the ventricles, especially of the fourth ventricle, 
was granular. The third case was admitted in a maniacal 
condition, continued very aggressive, and was kept in a 
padded room, subsequently passing rapidly into a demented 
paralytic condition, and exhibiting after death the same con¬ 
dition of the cerebrum as the other cases. All five cases 
were emaciated at the time of death. Case 7 was diagnosed 
as mania; death occurred from peritonitis after operation 
for pancreatic cyst. Case 8 was also maniacal, and had 
advanced pulmonary phthisis with tubercular pyelitis. No 
macroscopic change in the brain was noted after death in 
these two cases beyond post-mortem staining and congestion 
of the cerebral cortex. Case 9 also had advanced pulmonary 
phthisis ; at the autopsy the pia arachnoid was found to be 
white and opaque over the vertex and frontal lobes, and its 
meshes contained clear yellow fluid, the ventricles also con- 



taming an excess of fluid. Case 1 was killed on the railway 
and was in perfect health at the time of death. It is a 
matter of regret that only a single perfectly healthy case has 
so far been examined. It is, however, extremely difficult to 
obtain absolutely normal fresh brains. 

In the microscopical examination of these cases a portion 
of the paracentral lobule was stained by Nissl’s method, 
and another portion of the same part of the cortex was 
hardened in Muller’s fluid and stained by Marchi’s and 
Schaefer’s methods. In the cortex of the hemispheres of 
the general paralytics perivascular cell-infiltration was pre¬ 
sent, with dilation of the perivascular lymph-spaces, chroma- 
tolytic changes were present in many of the nerve-cells, and 
a variable degree of degeneration of fibres was observed 
[Table I.j. In the seventh, eighth and ninth cases also evi¬ 
dence of both chromatolysis and of fibre degeneration were 
found. The first case appeared normal on microscopical 
examination. In consequence of the large extent and com¬ 
plexity of the cerebral hemisphere and of the impossibility 
of removing more than a small amount of its substance 
without running the risk of altering the chemical composition 
of the remainder, the microscopical examination is neces¬ 
sarily defective, and, owing to the smallness of the area 
sectioned, some hesitation must be felt in forming a general 
judgment as to the condition of the hemisphere as a whole. 

In addition to the cerebral hemispheres just described, 
eight spinal cords were selected for the estimation of water 
and phosphorus [Table II.]. Seven of these were from 
typical cases of general paralysis, one running an acute 
course; and the remaining spinal cord was a perfectly 
healthy one, taken for comparison. As will be seen from 
the numbers attached to the cases, some of the spinal cords 
were taken from subjects whose cerebral hemispheres had 
also been submitted to chemical examination. There was, 
excluding the first cord, but little alteration in the naked- 
eye appearance of these cords beyond an excess of fluid in 
the sub-arachnoid space and a slight opacity of the arach¬ 
noid membrane. The microscopical examination of the 
spinal cord is fortunately far more readily made than is that 



of tbe cerebrum, and the information thus obtained is much 
greater and more precise than that afforded by the clinical 
notes. As in case of the cerebral cortex, the methods of 
staining employed were those of Nissl, Marchi and Schaefer. 
On reference to Table II., where the results of the micro¬ 
scopical examination of the cervical region are briefly tabu¬ 
lated, it will be observed that in all the cases except the first 
there was some degree of degeneration, rarely, however, of 
considerable extent, and most frequent in the pyramidal 
tracts. In three of the affected cords the condition of the 
chromoplasm was noted; in two cases there was a slight 
degree of chromatolysis ; in the remaining case the chromo¬ 
plasm of the anterior horn cells appeared normal. 

Chemical Examination of the Cerebral Hemispheres 
and Spinal Cords. 

Mention has already been made of tbe marked wasting 
of the brain in the cases of general paralysis. On reference 
to Table I. the extremely low weight of the hemispheres in 
these cases is to be noted. In all these cases the cerebro¬ 
spinal fluid had undergone a correspondingly large increase. 
Thus in Cases 3, 4 and 6, respectively, 120 c.c., 130 c.c., and 
115 c.c. of cerebro-spinal fluid were collected, but this did not 
represent the whole amount present. In Case 9, in which 
was also an excess of cerebro-spinal fluid and marked wast¬ 
ing of the cerebrum, the weight of the hemispheres was very 
small. In Cases 7 and 8, in which there was no excess of 
fluid, the weight of the hemispheres is considerably higher. 

The percentage of water in the cases of general paralysis 
was from 3 per cent, to 5 per cent, higher than in Case 1, 
which was normal. In Case 9, as might be expected from 
the excess of cerebro-spinal fluid which was found, there was 
again a high percentage of water. These results are in 
accord with the dilatation of the perivascular lymph-sheaths 
which was observed on micrcosopic examination in these 
cases. In Cases 7 and 8, in which, as just mentioned, the 
brain was dry in aspect, the percentage of water contrary to 
what might be expected was also found to be considerable. 



No exact quantitative relation could, however, be ob¬ 
served between the amount of increase in the percentage 
of water and the degree of wasting of the hemispheres, nor 
could any definite relation between the former and the age 
of the patient be traced. 

Turning now to the estimation of phosphorus, the first 
point that claims attention is the fact that, as the percentage 
of the element is not increased in amount in the cases of 
general paralysis, in which considerable wasting of brain 
tissue had taken place, there has occurred a large actual loss 
of phosphorus proceeding pari passu with the loss of cerebral 
substance. The same is also true of Case 9. The conclusion 
to be drawn from this is that such dissolution of nerve-tissue 
as takes place rapidly becomes complete, no constituent 
remaining behind. 

The percentage of phosphorus in the dried hemispheres 
in the various morbid conditions examined was but little 
different from that occurring in Case 1, such variations as 
were found consisting, with one exception (Case 2), in a 
slight defect of phosphorus. Although this variation in 
percentage is small, it must be recollected that, as the 
phosphorus holding fatty and proteid substances present in 
nervous tissue are of very complex composition, the actual 
amount of nerve substance which is thus indicated as having 
undergone alteration may be by no means inconsiderable. 

On reference to Table I. it will be seen that, putting aside 
Case 2, in which no microscopical examination was made, in 
all the affected hemispheres degeneration of nerve-fibres and 
chromatolytic change in nerve-cells were observed. Both 
these changes varied in degree in different cases, as is indi¬ 
cated by the description in the table. There is, however, no 
quantitative relationship between these structural changes 
occurring in the nerve fibres and nerve-cells of the paracentral 
lobule and the lowering of the percentage of phosphorus. 
It will be noted that in Case 2, in which an extreme degree 
of wasting of the cerebrum occurred, the percentage of 
phosphorus did not differ from that found in the healthy 
brain of Case 1. It may be mentioned in this connection as 
bearing upon the smallness of the variations in the percentage 



of phosphorus that the changes present in degeneration of 
some standing were, in another research, found to be 
attended with less deficiency of phosphorus than when the 
degeneration was quite recent. 

It is also to be noted that, although there is a correspon¬ 
dence between the deficiency of phosphorus in the affected 
hemispheres and the high percentage of water which is 
present, this relation is merely qualitative; the variation is 
not of the same degree in the same cases. Similarly there 
is no simple quantitative relationship between the defect of 
phosphorus and the degree of wasting of the brain or the 
age of the patient in the cases of general paralysis. 

In the cords examined the separation from the cerebrum 
was not in most cases made accurately between the hypo¬ 
glossal and sub-occipital nerves, the brain having been 
removed before the spinal cord was exposed, so that the 
total weight of the individual cords cannot, unfortunately, 
be given. 

In the seven cases of general paralysis recorded in Table 
II., the percentage of water in the spinal cords was from 
*5 per cent, to 3’4 per cent, higher than that found in the 
healthy spinal cord of Case 1. In this respect the condition 
of the spinal cord agrees with that of the cerebral hemi¬ 
sphere in general paralysis, though in the latter the increase 
in the percentage of water is higher than in the spinal 

On contrasting Tables I. and II. it will be seen that no 
quantitative relationship can be traced between the increase 
in the percentage of water in the spinal cord and that oc¬ 
curring in the brain, or between the former and the degree 
of wasting of the cerebral hemisphere in the three cases 
(4, 5, 6) in which the comparison can be made. Nor can 
any definite relation be found between the percentage of 
water in the affected cords and the age of the patient. 

The percentage of phosphorus in the affected spinal 
cords exhibits variations which are not generally greater 
than those occurring in the affected hemispheres, though in 
one case (13) the percentage falls as low as l - 28. In con¬ 
nection with this latter, reference may be made to a de- 



generated cord, particulars of which are given elsewhere, in 
which also the percentage of phosphorus in the whole cord 
fell to 1*28. With a single exception (Case 10) the altera¬ 
tion in the percentage of phosphorus in the affected cords in 
Table II. was always lowered. 

On microscopical examination there was found, as in the 
hemispheres examined, evidence of tract-degeneration, and, 
in two cases, of chromolytic changes in the nerve-cells; but 
the extent of these structural alterations does not appear to 
correspond quantitatively to the degree of variation in the 
percentage of phosphorus. Some explanation of this want 
of correspondence is afforded by the work to which reference 
has just been made in which the variation of the percentage 
of phosphorus was found to be greater in quite recent than 
in old degeneration. 

Although, except in Case 10, the decrease in the per¬ 
centage of phosphorus is attended by an increase in the 
percentage of water in the affected cords, no quantitative 
relationship between the two can be recognised. Simi¬ 
larly, no close correspondence can be observed between 
the percentage of phosphorus and the age of the patient, 
and on contrasting Tables I. and II. no direct relation¬ 
ship between the diminution of phosphorus in the cords 
of Cases 4, 5 and 6 on the one hand, and the defect 
of phosphorus in, or the wasting of, the corresponding 
hemispheres can be observed. 

The Work of Gutnikov. 

So far as I know the only other observer who has studied 
the percentage of water and phosphorus in the brain in 
various morbid conditions is Gutnikov, whose very in¬ 
teresting paper has already been referred to. This observer 
examined grey and white matter separately and also esti¬ 
mated nitrogen and sulphur in each. Although Gutnikov’s 
results are not strictly comparable to mine, owing to his 
separation of grey and white substance, nevertheless the 
wide variations in the percentage of phosphorus which he 
obtained in different conditions are difficult to reconcile with 



the comparatively small differences which I have found in 
the hemispheres I examined. Thus, in the brains of 
foetuses Gutnikov found 11 per cent, to 2T per cent, of 
phosphorus ; in healthy adults from 8 per cent, to T5 per 
cent, of phosphorus in the grey matter and from *7 per cent, 
to 17 per cent, in the white matter; while in various 
morbid conditions the following was the percentage of 
phosphorus in the grey matter of the cortex :— 

Epilepsia somatica 

1-67 per cent. 

Melancholia passiva ... 



Mania tranquilla . 


9 > 

Idiotismus . 


9 9 

Pseudo-paralysis syphilitica ... 


9 9 

Dementia post-epilepsiam com- 

binatam . 



Dementia post-maniam 



Dementia senilis . 


r f 

Dementia paralyti ca ... 





y t 

Dementia senilis . 






and similar variations were found in the white matter. 

The excellent method which Gutnikov used for the 
destruction of organic matter was adopted in my analyses. 
The further procedure was, however, different, for Gutnikov, 
in estimating phosphorus, titrated with uranium nitrate. 
The separation of grey and white matter which Gutnikov 
adopted perhaps introduces some risk of error in estimation, 
while it also reduces the amount of material which can be 
obtained for analysis. 


(1) The cerebral hemispheres were found to be con¬ 
siderably diminished in weight in the advanced cases of 
general paralysis of the insane examined, the cerebro-spinal 
fluid undergoing a proportionately large increase in the 
ventricles and sub-arachnoid space. The same was also true 
of the case of alcoholic dementia. 



(2) In general paralysis of the insane and in the other 
morbid conditions studied, there was found an increase in 
the amount of water present in the cerebral hemisphere, 
not only in those cases in which the cerebro-spinal fluid was 
markedly in excess, but also in the two hemispheres in 
which no such marked excess of fluid was observable. 

(3) No definite relation could be found between the per¬ 
centage of water and the degree of wasting of the cerebrum 
or the age of the patient. 

(4) The phosphorus contained in the cerebral hemi¬ 
spheres in the cases of general paralysis of the insane under¬ 
went an actual diminution, corresponding very closely to 
the wasting of the hemispheres, so that— 

(5) The percentage of phosphorus in the dried hemi¬ 
spheres was but little altered, such alterations as occurred 
being in the direction of a diminution. 

(6) This diminution in the percentage of phosphorus 
was associated in all the cases examined with evidence of 
nerve-degeneration and of chromatolysis, but there was 
no definite correspondence between the two as regards 

(7) Although the increase in the percentage of water was 
accompanied by a decrease in the percentage of phosphorus, 
the former was not directly proportionate to the latter. 
Nor did the defect of phosphorus stand in any direct relation 
to the age of the patients or to the degree of wasting of the 
hemispheres in the cases of general paralysis. 

(8) In the spinal cords examined there was found in 
general paralysis of the insane an increased percentage of 

(9) No definite quantitative relation existed between 
this increased percentage of water and the age of the 
patients, or the increase of water or the wasting of the 
corresponding cerebral hemispheres in the few cases in which 
this comparison could be made. 

(10) The percentage of phosphorus in the dried cords 
was generally diminished, the extent of the diminution, with 
one exception, not exceeding that met with in the hemi¬ 
spheres examined. 



(11) The diminution of the percentage of phosphorus in 
the cords of general paralytics was in all cases associated 
with evidence of tract degeneration, and in some of the 
cases with slight chromatolysis in the anterior horn-cells. 
The correspondence between the two, however, as regards 
degree is not very precise. 

(12) The increase in the percentage of water in the 
affected spinal cords was accompanied, with one exception, 
by a diminution in the percentage of phosphorus, but the 
former was not directly proportionate to the latter. Nor 
could the decrease of phosphorus be correlated to the age of 
the patient or to the wasting of the corresponding cerebral 
hemispheres or their defect in phosphorus and their in¬ 
creased percentage of water in the three cases in which this 
comparison could be made. 


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At the suggestion of Dr. Mott, I have during the 
year 1897 undertaken an investigation of the part played 
by syphilis in the causation of insanity, and part of the 
results, namely, those in connection with general paralysis 
are here stated. 

The method of investigation has been this:—Taking 200 
consecutive cases admitted into Claybury asylum, I found 
some evidence of their having suffered from venereal infec¬ 
tion in seventy-one instances. Out of these 200 cases there 
were twenty-three general paralytics, and of these sixteen 
presented absolute evidence of syphilis, four cases doubtful 
evidence and three cases no evidence. 

In an investigation of this nature there are two special 
difficulties, that of obtaining evidence of syphilis, and that 
of deciding what cases to consider general paralytics. I 
have therefore written out the cases in full and appended 
a table containing an analysis of their symptoms. 

Touching the difficulty of obtaining evidence of syphilis 
in the pauper insane, it must be remembered that the first 
source from which evidence is to be obtained, the patient 
himself, is in most of these cases unreliable, as he is gener¬ 
ally more or less demented, and that the second source of 
evidence, the friends or relations, is also uncertain, for many 
of the patients are not visited ; these facts, in addition to 
the reticence which always exists both in patients them¬ 
selves and their friends on this subject, reduces the number 
of cases, in which a valuable history can be obtained, to a 
minimum. On turning to the objective signs, one is again 
met by peculiar difficulties because of the rarity of tertiary 



lesions in affections of the nervous system, attributable to 
venereal disease; indeed, the only one which I have found in 
such frequency as to be of much value is the scars of ulcers 
on the legs, and this can only be considered of value when 
taken in conjunction with other evidence. In each case I 
have sought with care for the presence of a penile scar and 
for the typical hard, shotty inguinal glands which often 
persist for years after the chancre has healed. 

It will be found in many cases that the history is very 
imperfect, but what it may lack in completeness which is 
unavoidable for reasons given above, I have tried to make up 
for in accuracy. 

On analysis the following facts appear:—Eighteen patients 
were married; fifteen were under 40 years of age and the 
remaining seven under 50, the minimum age being 30 and 
the maximum 49; in twelve cases some hereditary taint was 
discovered; sixteen cases were distinctly town-bred, two 
had lived a roving life and in two cases their previous abode 
was not known; in eleven cases patients had shown signs 
of ability; in seven cases there was a history of severe injury 
to the head; in six cases the patient had been in one of 
the services; in five cases there was a history of gonorrhoea ; 
sixteen of the patients were of dark complexion; in only 
two cases was the patient a habitual drunkard, and fifteen 
cases were distinctly abstemious. Every patient had some 
iridoplegia, every patient had some slurring of speech, in 
two cases there was no tremor of hands, face or tongue ; in 
fifteen cases the reflexes were exaggerated, in eight dim¬ 
inished; in no case was the specific gravity of the urine 
below 1020 (in two cases it was not noted); in eleven cases 
there was no seizure; in four cases one only, and in two 
cases two only ; in seven cases there was a ravenous appetite, 
and in six of these there was marked emaciation, in only 
one case was the appetite bad (and in this probably owing 
to delusions); in seven cases constipation was present; in 
every case there was more or less dementia; fourteen died 
within a year of their admission. 

The fact that fourteen patients were married is not par¬ 
ticularly significant, as they were all over 30 years of age ; 


that thirteen cases were under 40 bears out the rule that the 
disease generally begins in the thirties, and not infrequently 
has run its course before 40 ; a supposed general paralytic 
over 50 should be looked upon with suspicion ; to find some 
neuropathic history seems the rule rather than the excep¬ 
tion. Our patients being drawn from an urban population, 
the proportion of town-bred is not surprising. A majority 
of general paralytics have a history of previous mental 
acuity; there are, however, two remarkable exceptions (12 
and 19) 1 in which the original mental condition was amentia, 
and exceptionally one does see cases of general paralysis 
occurring in the weak-minded who are not congenital 

A history of injury occurs with sufficient frequency to 
point to its importance as an exciting cause, and this fact is 
perhaps best shown in Cases 14 and 2, where the disease, 
which ran a particularly rapid course, started very definitely 
from head injuries; it is significant that only two patients 
were drunkards, and the rarity of a history of drunkenness 
in general paralytics is a useful point to remember in the 
diagnosis between these, in an early stage, and cases of 
alcoholic insanity. 

Iridoplegia, slurred speech, alteration of the reflexes, 
tremor of the face, hands, and tongue are, I believe, the 
four cardinal physical signs of general paralysis: iridoplegia 
occurs in three forms—(i.) the unequal pupil, due to one 
pupil not reacting to light so efficiently as the other, and 
often refusing also to react to accommodation (3, 4, 5, 6, 8, 
11, 13, 15, &c.); (ii.) pupils with sluggish reaction, i.e., such 
as do not react readily to ordinary daylight, but will do so 
under the influence of a strong light, as a sixteen candle- 
power electric lamp (1, 2,10,12,19); (iii.) the typical Argyle 
Robertson pupil, reacting to accommodation but not to 
light, and associated with diminished knee-jerk, and often 
other symptoms of locomotor ataxy (7, 9). Irregular pupil 
has been noted in many instances (2, 5, 9, 14, 16, 17), and 
is of two kinds, one in which the pupil is oval (2); another, 
in which the pupillary edge presents an uneven margin (9). 

1 The numbers in brackets refer to the numbers of the cases given. 




All cases due to synechiae are, of course, excluded. Slurred 
speech varies widely in degree, from a slight hesitancy in 
saying long words (13) to an inco-ordination so marked that 
the patient can hardly make himself understood (6, 16). 
Tremor varies both in degree and quality, but is usually of 
the nature of an intention tremor, best seen when an 
attempt is made to write or draw a long line with a fine- 
pointed pen; it was only absent in two cases (12 and 15); 
was sometimes excessive (11, 6), sometimes hardly recog¬ 
nisable (4, 10). The reflexes are usually exaggerated, and 
ankle clonus and wrist-jerk are not infrequent: the knee- 
jerks may be diminished when no other sign of ataxy is 

The high specific gravity of the urine is, no doubt, 
associated with the altered metabolism which causes the 
“ ravenous appetite ” and the “ extreme emaciation.” 

In eleven cases there was no seizure, and seizures appear 
rather as an incidental symptom, perhaps due to the ac¬ 
cumulation of deleterious matters in the blood in large 
quantities, than as a regular feature of the disease; it is not 
uncommon to find a seizure at the commencement of the 
disease (2, 8, 12), or at its termination (4, 10, 14)—one 
might say, terminating it, and that often prematurely 
(10, 19). 

Definite symptoms of gastro-intestinal disturbance are 
wonderfully uncommon, considering that these patients bolt 
their food and take no exercise, and here existed in only one 
instance (18), and then was associated with delusions of 
poisoning. Constipation is common, but not tbe rule, and 
appears to bear no definite relation to the presence of 
seizures. Trophic sores, by which I mean a small vesicle, 
often in a part not subject to pressure, rapidly breaking 
down into an ulcer with a sloughing, unhealthy base, are 
uncommon, and occur in only one case (2). Insomnia is 
frequently noticed at the commencement of the disease, 
Case 10 forming a striking exception to this rule. 

That fourteen cases died within a year of their admission 
shows the rapid course which typical general paralysis runs, 
and that this must be taken to indicate the length of their 


illness in every case, for of those that died, the history in 
some cases (5) extends back for four years ; while in others 
(14) the whole course of the disease was run in four months. 
In several instances (11) anti-syphilitic drugs were exhibited, 
but without success. 

The mental aspect of these cases illustrates what is usual 
in general paralysis, the presence of dementia of a progres¬ 
sive character; whatever else may be present, the only 
constant factor is this dementia, and any temporary im¬ 
provement of it is rare. The only cases in which this was 
not marked were 5 and 13; in the former the patient, whose 
condition was always that of exaltation, died prematurely of 
exhaustion and probably before dementia had become well 
developed ; in the latter his dementia is practically at a 
standstill. Not only is dementia the keynote of the whole 
mental condition of these cases, but is frequently the first 
change observed (6, 10, 11) and often the only one noted 
(15, 9). In studying the first mental alteration, cases fall 
naturally into two groups, the more chronic form, which 
commences slowly and insidiously with lapses of memory 
and other signs of dementia, associated sometimes with 
depression (2, 16), sometimes with exaltation (3, 5, 9, 13), 
sometimes with irritability (8, 15, 18), sometimes with 
hallucinations (10), and the more acute form, which begins 
with an outburst of maniacal excitement (7, 14). It is 
occasionally seen that the patient has been of a neurotic 
disposition (3) or degenerate type (12,19) all his life. From 
time to time one sees patients who after a short stay in the 
asylum obtain their discharge as recovered, only to return 
with well-marked symptoms of general paralysis, and it 
seems not improbable that there are certain mental states 
which are more liable than others to develop into general 
paralysis and which may be considered as fore-runners 
of that disease and should be looked upon as fore-wamers 
of it. 

With regard to the mental progress, egotism, bien etre, 
undue emotionalism, delusions of grandeur (3, 4) or perse¬ 
cution (1,8), and hallucinations of sight (8) or hearing (9) are 
frequently seen; but while these conditions alternate with 



one another so as to produce a strange medley of symptoms, 
so that while suffering from delusions of persecution a 
patient at one time in an excess of exaltation boasts of 
how he will outwit his persecutors, at another is wrapped 
in the deepest melancholy because he sees no loop-hole of 
escape, the steady progress of his dementia may still be 
seen in the character of his delusions, which at first form 
an intelligent tale but later become a string of incoherent 

January, 1899. 

Case 1. 

J. F., aged 49, married ; manager of a factory. 

Family history .—He is one of a family of drunkards. 

Personal .—Lived most of his life in London. During early life 
worked very hard and succeeded in attaining to a post of manager of a 
large candle factory. Has spent much time in educating himself and 
acquiring a more intimate knowledge of that chemistry which is con¬ 
cerned in candle making, and apparently had spent some time in experi¬ 
menting with a view to cheapening the processes now in vogue. As a 
young man lived a steady life and had been a regular churchgoer. Has 
always been a teetotaler. Gives a history of syphilis (chancre, followed 
by rash and sore throat); presents no tertiary symptoms. Married 
when 27. Before admission had been overworking and had had an 
attack of influenza. Had been noticed to have been strange in his 
manner for about a fortnight. 

Present illness .—Was admitted on February 27, 1897. His mental 
ideation and reaction to questions slow. Memory for recent events poor, 
for remote fair. At times semi-incoherent and has difficulty in con¬ 
centrating his attention. He is exalted, filled with ideas of his own 
genius and importance, but at the same time exhibits well-marked de¬ 
lusions of persecution such as that he is surrounded by telephone wires 
and that there is a plot on foot to blow him up with dynamite. 

Pulse 108, small, regular. Urine 1030, acid, no albumen, no sugar. 
Sight, K. L. J; pupils irregular, unequal (L. larger); react slowly to 
both; nothing abnormal in fundus. Slight discharge from the ears. 
Cannot hear w T atch placed close to either ear, but hears it readily when 
placed between the teeth. Touch acute. Co-ordination good. Well- 
marked tremor of face, tongue and hands (well exhibited in hand¬ 
writing). Reflexes exaggerated, but no ankle clonus. Muscular power 
poor. Speech hesitating, slurred ; difficulty in pronouncing r’s and in 
saying any words of many syllables. He appears to be very erotic. 
Nothing else to note in his bodily condition. 


Progress. —While here there was some increase in the degree of his 
dementia and he never showed the least sign of improvement, but was, 
unfortunately, transferred to another asylum after being under observa¬ 
tion a little more than a month. I learn, however, that after getting 
progressively worse, he died on June 9, 1897. 

Case 2. 

D. McK., aged 88, married ; a clerk. 

Family history. —Intemperance on father’s side. 

Personal history. —Born in Dublin ; has lived in various parts of the 
British Isles, and was for two years in the army in India. When a lad, 
was always fond of reading and mathematics. Acted as an assistant school¬ 
master in the army, and since then has been a clerk. Always reserved 
and quiet. Always been a teetotaler. Had syphilis when 24 (chancre, 
rash and sore throat). Married when 80. No children. In October, 
1896, had a fall down some steps, striking the back of his head and 
causing unconsciousness. 

Present illness. —In the beginning of January, 1897, was noticed to 
be strange and imaginative, forgetful, showing lack of confidence in 
himself, and hesitancy in business affairs. Seemed to lose all his energy 
and to suffer from insomnia, and to lose flesh, though his appetite was 
normal; he then acquired delusions of suspicion about his wife; thought 
at times that he had two or three wives ; had lapses of memory, so that 
he did,not recognise his wife; became unduly emotional, crying without 
cause, and was at times depressed, and attempted suicide by strangula¬ 
tion. Later, he developed hallucinations of sight and hearing. During 
January he had two slight fits, causing loss of speech and memory for a 
few hours. Admitted here on March 8, 1897. His ideation and mental 
reaction was slow, his memory for recent events bad, and for remote 
ones fair. He had hallucinations of sight and hearing, and delusions of 
suspicion and persecution; he was depressed, and even slightly suicidal. 
He was rather childish and nervous, being easily startled by a slight 
noise ; was not irritable, but kindly disposed towards others; was in no 
way egotistical, and showed no sign whatever of exaltation; he was not 
incoherent, but rambling and long-winded in his statements; his mental 
arithmetic was accurate. Was inclined to be restless, picking at his 
clothes, and so forth. 

Pulse 64 ; soft, regular. Urine 1020, acid, no albumen. Sight good. 
Pupils equal, irregular (oval, with long diameter vertical), widely dilated, 
react slowly and imperfectly to light, better to accommodation. Hearing 
good. Touch acute, accurate. Co-ordination good. Muscular power 
slightly impaired on right side. Speech slurred and hesitating. Gait 
unsteady, with some dragging of right foot. Reflexes diminished. 
Marked tremor of face, tongue, and hands. Nothing else of importance 
to note. 

Progress.— Since admission he has rapidly and steadily lost ground, 
mentally and physically. In April his condition underwent a marked 
change; though he did not get stouter, he acquired a sense hien ctre y his 



delusions began to assume a grandiose character, he became exalted and 
egotistical to the last degree, yet, though so much concerned with his 
own affairs, he was quite unable to look after himself, being careless and 
untidy in his dress, wet and dirty in his habits, and easily taken advan¬ 
tage of by other patients in the ward. A striking feature in this part of 
his progress to utter dementia was the constant and rapid variation of 
his delusions, so that now’ he is moving his legs about as a means of 
propelling the wonderful new steamboat he has invented, and anon, 
thinking he is some person of great importance, is seen behaving in 
what he considers an appropriate manner. While this change in his 
mental state is going on, it is possible to notice a steady increase in the 
depth of his dementia; day by day he becomes less able to answer 
questions intelligently, and by June is so demented that he cannot even 
answer the simplest questions. Lying in bed, he takes no notice of his 
surroundings, but remaining in the same position all day, taking his 
food well, steadily loses weight. On June 29 he died utterly demented 
and extremely emaciated. He developed several bed sores and a trophic 
sore on his arm, opening into the elbow f joint. 

Case 8. 

M. F., aged 85, married ; a commission agent. 

Family history .—His mother was a highly neurotic woman. 

Personal .—Born in Turin ; till 16 he lived in Italy, since which time 
he has lived chiefly in London. Went to school in Turin, but did not 
get on very w f ell there; was always very wild, continually getting into 
trouble on account of some jackanapes trick or other. In those days 
was always self-willed, conceited and inclined to over-rate his importance. 
Although he has been in the wine trade, has always been a most 
abstemious man. Had syphilis when about 20 (brother gives good 
history and there is penile scar). Married when 28; his wife had one 
miscarriage but no children ; was a successful man and clever at his 
business and held some good positions, but was inclined to speculate 
unwisely. He has suffered much from insomnia. Has alw T ays been 
of an affectionate and erotic disposition. 

Present illness .—For some years he has been of a suspicious tempera¬ 
ment and has attempted suicide in moments of impulse, though he has 
never been particularly depressed; the first occasion being an attempt to 
jump from an hotel window when he was 24 years of age. He also was 
eccentric in manner and had a great mania for bringing home strange 
dogs and so forth. For the last two years a change has been noticed in 
his mental state ; he was continually starting some new scheme only to 
abandon it before completion ; often spending money in an absurd and 
extravagant manner ; not attending to his domestic and social duties ; he 
has shown frequent lapses of memory both for names and things and con¬ 
siderable exaltation. During this period his insomnia has been very trouble¬ 
some. For the last five weeks he has become much worse, his condition 
being aggravated by poverty and lack of food; he has developed well-marked 


delusions of grandeur and wealth, has become both violent and suicidal, 
has had difficulty in speaking distinctly and a more and more marked 
loss of memory. Was admitted on March 19, 1897. Exalted, excited 
and garrulous, he says that he has .£45,000,000 and is Baron Brunati 
and that he is distinguished for his cleverness, strength and goodness; 
his conversation is in the superlative degree and he is intensely egotistical, 
inclined to be aggressive, continually shouting and muttering to himself ; 
he has many and constantly varying delusions; he has marked loss of 

Pulse 80, regular, fair volume. Urine 1,020 acid, no albumen. 
Sight good; pupils unequal (R. larger), regular; react slowly and 
imperfectly to light and accommodation. Hearing good. Touch rather 
dull in lower extremities. Co-ordination good. Speech, slurring of many 
words. Muscular power fair. Gait steady ; reflexes exaggerated; 
tremor of face and hands. Nothing else of importance to note in his 
physical condition. 

Progress .—While here has steadily got worse, becoming more de¬ 
mented and losing weight rapidly; his inco-ordination is excessive ; his 
speech is so bad now that it is almost impossible to understand what he 
says; he gradually is losing his exaltation and grandiose delusions, is not so 
egotistical and does not talk of any schemes for the future as he used to 
do; still he retains his sense of bien etre ; is extremely emotional but 
not depressed; his dementia is such that, though he knows his name and 
remembers the fact that he is married, he has no idea of his age or how 
long he has been here. It is interesting that, while he was still able to 
talk English fairly fluently he has quite lost his power of talking his 
native language, Italian; whether this is to be attributed to his inco¬ 
ordination of speech or his dementia it was not easy to tell. Does not 
suffer from headache. He lost mental and physical strength, and died 
from exhaustion on September 18, 1898. Never had a seizure. 

Case 4. 

H. W. B., aged 80, single ; a carman. 

Family history .—Nothing known of his family history. 

Personal .—He states that he used to be fond of school and got a 
prize for drawing and that he has never been addicted to drink. States 
that he has had syphilis (has a small scar as of an abscess in the groin); 
constantly boasting of his successes with women ; he is evidently very 

Present illness .—When admitted here, March 20, 1897, he was very 
noisy, restless and exalted ; states that he is very strong and very clever, 
that he has built a church and has thousands of pounds in the bank, 
that he had a fight with a celebrated pugilist and beat him. He is 
unduly emotional, crying and laughing without cause; he has a fail- 
memory for remote and recent events. 

Urine 1080,' acid, no albumen, no sugar. Pulse 64, regular, good 
volume. Pupils regular, unequal; (L. larger) ; both react to light and 



accommodation fairly. Reflexes increased; slight tremor of the hands, 
none of the face. Speech indistinct and slurred; cannot pronounce words 
of many syllables. He is markedly aneemic. Never complained of 

Progress .—He lived until June 15, and during that time was at first 
very restless, constantly wandering about, picking at his clothing and at 
times destroying it, rapidly becoming more feeble and less inclined to be 
aggressive; he remained very exalted and egotistical. Towards the end 
of April he had become much more feeble both mentally and physically, 
and, though he was on extra diet and took his food ravenously, he con¬ 
tinued to lose weight and strength. By the end of May he was very 
emaciated and showed considerable increase of his dementia, but retained 
much of his exaltation; thus impelled by delusions of his great strength, 
he would fight with other patients when he was hardly able to walk 
without assistance. From this time his dementia became so gross that 
he no longer could give any coherent account of his feelings and was 
unable to answer even the simplest questions. He was extremely wasted 
and on June 14 had two seizures from which he never rallied. Died 
from exhaustion on the 15th. 

Case 5. 

A. W. T., aged 88, married; a solicitor. 

Family history .—One of his relations died from paralysis. 

Personal .—Usually of a cheerful disposition, never a heavy drinker; 
definite history of syphilis (has chronic glossitis and scars in groin.) 

Present illness .—First admitted on October 8, 1895, and then had 
been noticed to have been strange in manner for two years, and had 
suffered from insomnia for some months. He was violent, excited, 
unduly emotional, exalted, impulsive, erotic, and had delusions of per¬ 
secution. His speech was hesitating, but not definitely slurred; his pupils 
unequal (R. larger) and irregular; his reflexes were exaggerated; he took 
his food well, but not ravenously ; was not defective in his habits. While 
here was at first noisy, aggressive, and developed grandiose delusions, 
but was discharged on December 81, 1896, being more demented, and 
hence quieter, but not otherwise improved. He was re-admitted March 
26, 1897, incoherent, noisy, violent, exalted; he had delusions of perse¬ 
cution, such as that he was watched by detectives, and that his food was 
poisoned, and had also hallucinations of sight and hearing. He was so 
restless that it was impossible to examine him thoroughly, but he was 
thin, pale, with a dry brown tongue, sordes on the lips and constipated; 
his pupils were very contracted and his reflexes exaggerated; his speech 
was fairly distinct; tremor of hands and face. 

Progress .—Notwithstanding the fact that he was put on extra diet 
and was given trional and paraldehyde in full doses, he remained de¬ 
structive, noisy, and troublesome, until two days before his death, which 
took place on April 20 from exhaustion, all efforts to keep him quiet and 
procure him some sleep being unavailing. He never had any seizures. 


Case 6. 

J. B., aged 88, single; a seaman. 

Family history .—No history of insanity, alcoholism, or phthisis. 

Personal .—He was bom in London, but, owing to his occupation, he 
has never been resident in any place long. Always of a cheerful dis¬ 
position ; has never been a heavy drinker. Had syphilis when 25 (history 
of chancre, sore throat, bad eyes, &e.). Was treated for twelve months. 
Has had several severe accidents. 

Present illness .—Was admitted May 7, 1897, very demented, quite 
unfit to look after himself; incoherent, no knowledge of time or place, 
noisy, continually shouting a lot of incoherent nonsense; is not violent or 
suspicious, does not appear to have any aural hallucinations. 

He is very deaf. Urine 1020, acid, no albumen, no sugar. Pulse 80, 
regular, fair volume. Pupils unequal (L. larger), regular, react slowly to 
both light and accommodation. Reflexes much exaggerated, no ankle 
clonus. Tremor of face and tongue, but not of hands; paresis of lower ex¬ 
tremities. Inco-ordination marked. Speech slurred. Wet and dirty. 
Deep puckered scar posterior border of right axilla. Head measurement, 
C. 64, Ap. 29}, Bp. 15}, Bm. 14.* 

Progress .—At first somewhat noisy. He became gradually quieter as 
his dementia increased. He has some remote exaltation; he is emotional 
at times, laughs and chuckles to himself in a very pleased way, but as 
often cries, and even at times appears really depressed, saying that he is 
in a pitiful state, and would be better out of it; his progress is very 
gradual, but he is now thinner, more demented, and has to be carried 
about. Has had no seizure. 

Case 7. 

T. S., aged 87, married; a stevedore. 

Family history .—No history of insanity, alcoholism or phthisis. 

Personal .—Born and always lived in London. First went to work 
when 18. When a young man lived rather a fast life and confesses that 
he has been very erotic. Has never been a heavy drinker. Been rather 
a reserved temperament. Always successful at his work. Had syphilis 
when 21 (a clear history of chancre, sore throat and rash); has enlarged 
inguinal glands. Married when 80 ; no children. Has had gonorrhoea. 

Present illness .—On January 22, 1896, had a maniacal attack, which 
commenced with insomnia, grandiose delusions, lavish expenditure of 
money and great but impossible schemes for the future. He was 
admitted to this asylum on the 29th, noisy, excited, destructive and 
violent, continually boasting of his own powers, both physical and 
mental, and exhibiting well-marked expansive delusions, such as that he 
is a millionaire, &c. He was in good physical health. Had exaggerated 
reflexes, well-marked wrist-jerk, slurring of speech, dilated but equal 
and reacting pupils. During his stay of nine months he improved some¬ 
what, though he had several seizures, and a greater part of the time was 
noisy and violent, constantly fighting with other patients and so forth. 

* C. Circumference. Ap. Anteroposterior. Bp. Biparietal. Bm. Bimastoid. 



He was sent home at the earnest request of his friends, though very 
unstable and never got well, but became gradually more demented and 
feeble till re-admitted on June 80, 1897, when, though his exaltation was 
Btill present, he showed a marked degree of dementia, having but little 
idea of time or place, being able to give no account of his career since he 
was discharged. At times quite incoherent but usually able to answer 
most questions with fair intelligence. His memory for both remote and 
recent events was defective. He states that for some time he has been 
worried by loss of sexual desire and capability, which he attributes to his 
early excesses, yet he has well-marked sense of bien etre t is very jolly in 
manner and well disposed towards others, is by no means egotistical or 
hypochondriacal, indeed, has grandiose delusions, the tendency of which 
is to make others rich and successful. Thus he states that his brother 
has thousands of pounds and owns a street of houses. He is emotional; 
has no hallucinations. 

Urine 1020 acid, no albumen, no sugar. Pulse 80, regular. Vision 
(R. A, L. $)—fundus normal; pupils equal, irregular, present the 
Argyle-Robertson phenomenon. Hearing impaired. Head measure¬ 
ment. C. 56, Ap. 85, Bp. 15}, Bm. 14}. Dynamometer, 1 R. 95, 
L. 85. Appetite good; bowels constipated. Speech slurred; tremor 
of face and tongue. Reflexes absent. Touch much impaired in legs 
and very inaccurate. Is unable to distinguish hot from cold objects. 
Co-ordination of lower limbs bad, but of movements of the upper 
extremities good. A well-marked ataxic gait. Has suffered from in¬ 
continence of urine for some years. Has had lightning pains in legs, 
but never girdle pains, “ padded hoof,” or gastric crises. 

Progress .—He lived a little more than two months, and during that 
time was noisy and even inclined to be aggressive at first. His grandiose 
delusions never left him and his dementia did not sensibly increase. 
His appetite remained good, though never ravenous, and he did not 
become noticeably wasted; indeed, at the time of his death was well- 
nourished. He never suffered from headache. Sixteen days before his 
death he was brought to bed for the first time by a succession of 
seizures, after which he had retention, and a large quantity of urine was 
drawn off by a catheter. He then developed considerable oedema of the 
left leg with fluid in the knee-joint from thrombosis of the femoral vein. 
This, however, under the influence of belladonna fomentations and rest 
soon disappeared. Still he became weaker and more demented, so much 
so indeed that he could not recognise his wife and died without any im¬ 
provement taking place in his general condition. During the last ten 
days of his life he had an irregular temperature, for which there was 
nothing in his physical condition to account. 

Case 8. 

B. H., aged 80, married : a labourer. 

Family history .—His mother, who is still alive, is a very neurotic 

'That is, “grasp” of right and left hands. 


Personal history. —Born and always lived in London ; he got on well 
at school, and when 18 first went to work. Since then has followed 
various occupations, but chiefly that of a mechanic ; he has been a clever 
man at his work, and has invented a number of small toys, whistles, and 
similar things. He led rather a fast life as a young man, and, though a 
teetotaler till he was 20, Bince then has drank rather heavily. He has 
always been self-willed and eccentric, and at times did not seem to have 
any control over himself. He was of an affectionate disposition and 
erotic. He has always been strong and energetic, and has never had 
any serious illness except syphilis, which he had when 10 (history' of 
chancre, &c., has penile scar and shotty inguinal glands, and scar of 
an old ulcer on the leg). He has had gonorrhoea. 

Present illness .—For the last three years has been irritable, and was 
noticed to have loss of memory, putting things away and forgetting 
where he had put them. In January, 1897, had a quarrel with the fore¬ 
man of the works where he was employed and got dismissed. Shortly 
after this had a fit, and since then has got progressively worse, his 
memory failing him more and more, and his behaviour becoming silly 
and childish; he has never been depressed, but always rather exalted; 
for some time before admission he had not slept well. Was admitted 
here on July 2, 1897, exhibiting a considerable amount of dementia with 
some loss of memory, and slow mental reaction and lack of intelligence 
in his answers to questions; at the same time he was very exalted, 
saying that he was very strong, and owned the biggest market garden in 
England, continually talking of what wonderful things he is going to do 
and of the various ways in which he intends to amass vast wealth. He 
is unduly emotional and extremely egotistical. 

Pulse 88, regular, good volume. Urine 1080, acid, no albumen, no 
sugar. Sight (R. j, L. —pupils contracted, unequal (R. larger), react 
badly to both; R. fundus normal, L. fundus central scotoma; numer¬ 
ous patches of choroidal atrophy surrounded by a pigment, especially in 
the macular regions ; a large atrophic patch on the temporal side ; disc 
normal. Speech slurred. Reflexes diminished ; marked tremor of face, 
tongue, and hands, well seen in his writing. Dynamometer, 140 each 
hand. Co-ordination impaired. Constipated. Hearing and touch good. 
C. 56, Ap. 86, Bp. 15, Bm. 13. 

Progress .—At first he was noisy and inclined to be quarrelsome, 
and his exaltation was much en evidence , but since, his dementia has 
steadily increased, so that he is quite incoherent at times, and he has got 
thinner and more feeble. He has at times had delusions and hallu¬ 
cinations, chiefly of a persecutory nature, such as that his wife is 
unfaithful, and that his room is full of rats and beetles; he is very 
irritable ; still he has retained his hien etre and exaltation, takes his 
food ravenously; never complains of headache; his speech is becoming 
more indistinct. He is emotional and cries a good deal; he sleeps 
well; is restless; at times becomes depressed and talks of committing 
suicide. After becoming grossly demented and extremely emaciated, 
he died from exhaustion, July 18, 1898. Never had a seizure while 



Case 9. 

II. R., aged 36, married; a bricklayer. 

Family history. —His mother was paralysed. A history of intem¬ 
perance on father’s side. 

Personal history. —He was born and has lived nearly all his life in 
London; was looked upon as a smart boy at school, and was successful 
at his trade in after life. First went to work when 13; has always 
been of a reserved temperament; was rather wild when a young 
man, and used to have a good deal to do with loose women; he has 
never been a heavy drinker; he enlisted when 22, and left the army when 
29; he was in a hussar regiment, and never went farther than Ireland, 
where he was stationed for a short time. Denies masturbation; has had 
gonorrhoea several times, had syphilis when 17 (a history of chancre, Ac., 
has penile scar and indurated inguinal glands); was treated at St. Bar¬ 
tholomew’s hospital for a few weeks. Married when 28; had one child 
which died at the age of 5, and seems to have been a hydrocephalic 
idiot. He has never had any severe accident; no history of poverty or 
business worry, and no domestic unhappiness except the death of his 

Present illness .—Has been strange in manner since 1896; full of 
schemes for the future, with grandiose ideas; self opinionated and 
egotistical; he exhibited frequent lapses of memory, often talking about 
things that had happened many years ago as if they had occurred only 
yesterday. He has never been depressed. Shortly before admission he 
wandered away from home and came back with his pockets filled with 
cabbages and all manner of strange things. He has always slept well; 
latterly has eaten ravenously, but lost flesh. Was admitted here on 
July 6, and examined shortly after admission; was found to be demented ; 
quite unable to recognise his situation; he had no idea of where he was 
or how long he had been here, or why he was brought here; was apa¬ 
thetic, dull, and unintelligent. Had auditory hallucinations; was not 
exalted, nor had any bien etre ; talked rather grandly about houses 
which he was going to build. 

Pulse 108, regular. Urine 1020, acid, no albumen, no sugar. Pupils 
contracted, slightly irregular, equal, react to accommodation, but not to 
light. Hearing and touch dull. Dynamometer, R. 120, L. 150. Co-ordi¬ 
nation good; speech distinct, no tremor of hands or face; reflexes 
diminished; bowels regular. Head measurement, C. 57, Ap. 37, Bp. 15J, 
Bm. 14. 

Progress. —Since here he has lost weight, and is becoming more de¬ 
mented, so that he does not know that he is married, and has no idea of 
his age; he shows no exaltation, no bien etre , no tremor of hands or 
face, and his speech is only very slightly affected; does not complain 
of headache; suffers from insomnia, and is restless and noisy at 
night. He died on October 24, 1898, after a succession of seizures ; 
in the previous month he also had a large number of seizures. His 
speech has never been much slurred, and he has only had slight facial 


Case 10. 

J. L., aged 39, married ; a clerk. 

Family history .—Mother died in a fit. 

Personal history .—He was born and has always lived in London; 
got on well at school. When 15, “ an orphan,” he had to shift for him¬ 
self, and got employment as an office boy, but by dint of his own 
exertions and capability became a lawyer's clerk when he was 20, and 
worked his way up to a good position against considerable difficulties. 
Was never of an excitable or nervous temperament, but rather reserved. 
When a young man lived a fast life and drank a good deal. Had syphilis 
when he was 25 (history of chancre; has scars of old ulcerations on 
legs); he was treated for about three months ; has no other illness. 
Was married when 34 (no children), and since then has been very steady 
and practically a teetotaler. 

Present illness .—In November, 1896, his conduct first became 
changed; he was always very anxious to go to sleep, and would go to 
bed very early; he had lapses of memory, and would make a muddle of 
his work, leaving out words and forgetting things that he knew well; 
he was very abstracted in manner, and had to give up work altogether 
in June, 1897. He then began to have aural hallucinations, and threat¬ 
ened to shoot his employer, who had always been very kind to him. 
During this time he lost weight considerably. Was admitted here on 
July 7, 1897. Somewhat exalted; he states that he is very strong and 
very clever, but at other times appears depressed; he is emotional, and 
cries without cause ; he exhibits considerable dementia, and has marked 
loss of memory for recent events. 

Pulse 80, regular. Urine 1020, acid, no albumen. Sight, hearing and 
touch good. Co-ordination good. Dynamometer, R. and L. 40. Pupils 
contracted, equal, regular, and react fairly to both. Very slight tremor. 
Speech slurred and indistinct; diminished reflexes; slight paresis of face 
on right side. Has a reducible L. oblique inguinal hernia. Head 
measurement, C. 56, Ap. 37£, Bp. 15, Bm. 12. 

Progress. —At first he was inclined to be aggressive, striking other 
patients in an impulsive manner; but later the progressive march to¬ 
wards extreme dementia and physical debility was well seen: he became 
wet and dirty, would sit in one place all day, was confused and took no 
notice of his surroundings, and had more marked loss of memory and 
gave less intelligent answers to questions put to him. He retained fair 
health, took his food with avidity, and slept well, but continued to lose 
weight until December 81,1897,.when he had a succession of epileptiform 
seizures, in which he died. 

Case 11. 

C. S., aged 43, single ; a hawker. 

Family history .—Nothing known. 

Personal history .—He was born in London, and has lived part of 
his life abroad (India and Egypt) as a soldier in the army. Got on 
fairly well at school, and went to work in some printing works when 12. 



Enlisted at 18, retired at 80. Since then has been a hawker. Had 
syphilis (history of hard chancre, sore throat, and rash ; has a penile 
scar, and shotty inguinal glands). 

Present illness .—Was admitted on July 8, 1897, suffering from de¬ 
mentia ; he was dull, semi-incoherent, apathetic, neglectful of himself 
and oblivious of his surroundings; has marked loss of memory, especi¬ 
ally for recent events. He exhibits no exaltation, but has well-marked 
aural hallucinations, chiefly of a persecutory character. He has attempted 

Urine 1020, acid, no albumen, no sugar. Pulse 80, regular, fair 
volume. Sight good, pupils unequal (R. larger), react sluggishly to 
light and accommodation. Touch and hearing good. Dynamometer, 
R. 100, L. 90. Knee-jerks almost absent. Tremor of arms, legs, lips 
and tongue. Co-ordination fair. Varicose veins both legs. Head 
measurement, C. 55, Ap. 84$, Bp. 15, Bm. 18}. Speech slurred and 

Progress .—He was an inmate here till December 26. when he died. 
During that time he became more and more demented, so that while at 
first he could tell you something of his history and what had occurred 
to him when out in Egypt, and so forth, latterly he was so grossly 
demented that he could remember little besides his name. He never at 
any time showed any exaltation or depression, nor was he unduly 
emotional or egotistical. His inco-ordination, especially in his legs, 
became very marked, and the tremor of his muscles extreme. He used 
to complain a good deal of headache, and, though unable to take any 
exercise, while he continued to take his food well, he lost weight con¬ 
siderably. On December 10 he had a seizure and never got up again; 
it chiefly affected his right side, but to some extent the left arm also. 
He remained unconscious to December 14 ; he then improved slightly, 
and even spoke, indistinctly, but became more and more exhausted, and 
died on the 26th. He had some retention of urine, and he was cathe- 
terised on the 18th and 21st. He was treated for some time by mercury 
inunction and potassium iodide in full doses by the mouth, but with no 
beneficial result. 

Case 12. 

W. R., aged 41, married ; a painter. 

Family history .—No insanity, alcoholism, or phthisis in the family. 

Personal history .—Born and always lived in London. Of a lively and 
cheerful disposition; lived a fast life and drank too much when young. 
Married when 26 (two children, alive and healthy). Had syphilis when 
80 (history of; has now penile scar ; scar in both groins). Always rather 
weak-minded, and, though not of a criminal type, was unfortunate in his 
companions, and was convicted for larceny and for receiving stolen 
goods several times, and finally was sentenced to seven years’ penal servi¬ 
tude in February, 1898. He went to Parkhurst prison, and was trans¬ 
ferred to Broadmoor Asylum on June 22, 1896. He was then in an 
advanced state of general paralysis, suffering from gross dementia. 
While there had several seizures. 


Present illness .—He was admitted here on August 6, 1897, deeply 
demented. He did not know his age, how long he had been here, where 
he came from; took no notice of his surroundings ; was incoherent; had 
some remote expansive delusions, and was often to be heard muttering to 
himself “ thousands and thousands of mountains,” and so on. 

Urine 1020, acid, no albumen, no sugar. Pulse 72, regular. Reflexes 
exaggerated; ankle clonus obtained. Pupils regular, react slowly to both 
light and accommodation. Muscular power poor. Speech indistinct; 
bowels constipated. Head measurement, C. 52, Ap. 82, Bp. 14J ; Bm. 
13. No tremor. 

Progress .—His dementia increased. He steadily lost weight, though 
he took his food always well, and towards the end very ravenously. 
Ultimately became so feeble that he had to be put to bed because he was 
unable to stand, and eighteen days later, on December 25, died in a state 
of extreme emaciation and utter dementia, grinding his teeth constantly 
in the latter days of his life. 

Case 13. 

G. H., aged 45, married ; a traveller. 

. Family history .—Nothing known. 

Personal history .—Born in Lancashire, and always travelled about a 
great deal. Since he was quite young he had lived a fast life. At an 
early age he was a bookmaker’s clerk and has been a successful card* 
sharper and professional billiard player. Has always had plenty of 
money, though he rarely came by it honestly, and, indeed, has belonged 
to the criminal classes almost all his life. Though from an intellectual 
standpoint very sharp, his moral sense was early blunted, and he now 
tells tales of how he has obtained money by cheating, and so forth, not 
only without shame, but with evident pride. Had syphilis when 17 
(history of hard chancre, sore throat and rash, and has now shotty glands 
and pigmented scars of old ulcers on both legs). Was only treated for a 
short time. Has had gonorrhoea. Has never been a heavy drinker. 
Married when 18 (had three children, all dead); married again when 
33 (three children, all alive). On December 19, 1895, was sentenced to 
three years* penal servitude and three years* police supervision for 
stealing. Was sent to Parkhurst, and subsequently transferred to 
Broadmoor on July 9, 1897, suffering from delusions of wealth and 
grandeur; full of his own importance and great capabilities. 

Present illness .—On August 5, 1897, was admitted here. He then 
exhibited marked dementia, being dull and unintelligent and having con¬ 
siderable loss of memory for recent events. He is exalted, shameless, 
egotistical, self-complacent, self-assertive and inclined to be lively and 
turbulent. He has a marked sense of hien Ure and is well-disposed 
towards others. He is much occupied with grandiose delusions; con¬ 
siders that he is the King of the Belgians and that the Prince of Wales is 
his brother; he thinks that he is enormously wealthy. He is a great 
collector of rubbish. 

Urine 1085, acid, no albumen, no sugar. Pulse 92, regular. Sight 



and touch good. Hearing somewhat dull in right ear. Pupils unequal 
(R. larger); react to light and accommodation imperfectly. Dynamo¬ 
meter, R. 85, L. 75. Reflexes increased. Co-ordination good; fine 
tremor of the hands. Head measurement, C. 57, Ap. 84, Bp. 15$, 
Bm. 14. Speech slightly impaired. 

Progress .—His exaltation remains unchanged as do his grandiose 
delusions, but he is now clean and tidy, works well in the ward, no longer 
collects rubbish, and is not aggressive. He takes his food well and 
sleeps well and never suffers from headache. His dementia is still 
marked, but not increased and he takes an intelligent interest in his 
surroundings, but his grandiose delusions are as prominent as ever; he is 
Prince Arthur, has enormous quantities of money, &c. The bien etre 
is still present; he is not irritable and is well-disposed to others; he is 
not losing weight. 

Case 14. 

H. W., aged 84, single ; a baker. 

Family history. —Mother died of paralysis. 

Personal history. —Was born and has lived nearly all his life in 
London. Got on well at school. Went to work when 12 as a baker’s 
boy and has always followed the trade of a baker since. He has always 
got on well, but never remarkably so. When young was somewhat 
unsteady and lived a fast life, having a good deal to do with loose women 
and occasionally drinking too much, but never could be considered to be 
a drunkard. Always of a cheerful disposition; never of a nervous 
temperament, nor until the present attack has he shown the least 
symptom of mental instability. He has not had any serious illness; 
has had syphilis (a penile scar and shotty inguinal glands). Has had 

Present illness. —Was in a row with some other men on August 28, 
1897, and received a blow on the head, which rendered him unconscious. 
On the 24th he was noticed to be strangely excited; he left his work and 
made the acquaintance of some girl, whom he drove about in cabs, 
sending the cabmen home to be paid. He said that he intended to take 
a summons out against his assailants of the previous night and bought a 
revolver with the confessed intention of shooting somebody. On Sep¬ 
tember 8, 1897, he w r as admitted in an acute maniacal condition—noisy, 
singing, dancing and shouting, exalted with w’ell-marked expansive 
delusions. He states that he can earn .£800 a week, is as strong as 
Sandow, is a wonderful genius, is a music-hall artist, is a patent baker, 
&c. He harps continually on the subject of a beautiful girl whom he is 
about to marry, the same, apparently, as he has lately been driving about; 
is evidently very erotic. He forms great plans for the future; is 
intensely egotistical and has well-marked bien Hre. 

Well nourished ; bruised from struggling and fighting. Urine 1080, 
no albumen, no sugar. Sight, touch and hearing good. Dynamometer, 
115 R., 90 L. Pupils irregular, unequal (L. larger), react slowly 
to both. Slight slurring of speech. Co-ordination good. Reflexes 


exaggerated; tremor of face and hands and tongue. Pulse 60, small, 

Progress. —Till his death, three months later, he became rapidly and 
progressively worse. For a time he maintained his exaltation, eroticism, 
restlessness, noisiness and destructiveness; never during the whole course 
of his illness was he depressed or hypochondriacal. At first he took his food 
well but not rapaciously. Under the influence of sulphonal (grains 20 
ter in die) he became somewhat quieter, but never completely so, and 
always slept badly. He never complained of headache, and, I learn, has 
never suffered from it. After a month he began to show some signs of 
dementia—lapses of memory, incoherency, &c.; he also was noticed to 
be getting much more feeble and to be losing weight, and he now began 
to eat his food ravenously and to try and obtain more (throughout the whole 
of his illness, it may be remarked, his bowels acted with regularity and he 
never suffered any kind of gastro-intestinal disturbance). His delusions 
persisted to the end of his illness and were always of the same grandiose 
or erotic type. About a month before his death he had a succession of 
twenty-eight epileptiform seizures (at this time he showed no rise of 
temperature, nor has he done so at all while here). On the three succes¬ 
sive days had a few seizures (two or three) each day. From this time 
his mental and physical deterioration was more marked, until he became 
before his death feeble and emaciated and grossly demented (though 
never so much so that he was unable to answer simple questions), while 
his grandiose delusions persisted to the last, as did his sense of bien etre; 
and his eroticism showed itself in the form of a perpetual flow f of the 
most indecent and licentious language and in the habit of masturbation. 
He died from exhaustion on December 9, 1897. 

Ca*e 15. 

W. J. K., aged 46, married; a hammerman. 

Family history .—Two paternal uncles committed suicide. There is 
a history of phthisis and intemperance on both sides of the family. 

Personal history .—Was bom and has always lived in London. He 
went to work when 18 in a blacksmith’s shop, and has always followed 
that occupation. Has been of a reserved temperament, has never been 
a drinker, has suffered from rheumatism. Had syphilis when 20 (history 
of chancre, and has scar on penis). Married w T hen 24; four children 
living, two dead. Some time ago had an injury to the head. Is said to 
have had an epileptic fit, at what age is not known. 

Present illness. —Was admitted on September 25, 1897. For twelve 
months previous had had lapses of memory at times, and at other times 
had been very passionate and even dangerous to others; had never 
suffered from insomnia or loss of appetite. On admission was suffering 
from dementia, his cerebration being slow and imperfect, and his memory 
for recent events bad; is excitable and inclined to quarrel and to be 
violent; is not exalted or egotistical, and has no grandiose delusions ; is 
not in any way depressed ; is unduly emotional. 

Urine 1020, acid, no albumen. Pulse 72, regular. Pupils unequal 




(R. larger), regular, react slowly to both. Reflexes exaggerated; no 
ankle clonus. Speech slurred, but fairly distinct. Co-ordination fair; 
no tremor of face or hands; is thin, suffers from flat foot, complains of 
headache. Dynamometer, R. 50, L. 55. 

Progress .—Since admission has been very restless, continually trying 
to get out of the door, picking at and destroying his clothes, but gradu¬ 
ally getting more demented; he now does not know where he lived, 
what work he used to do, or what his age is, and is incoherent; he also 
is losing weight, and has a ravenous appetite; he sleeps badly, spending 
his time at night rambling about his room muttering to himself; he 
retains some sense of bein etre. He shows no sign of depression or 
exaltation. Is continually grinding his teeth. 

Case 16. 

B. S., aged 35, married ; newspaper reporter. 

Family history .—There is no history of insanity, alcoholism, or 

Personal history .—Was born in Manchester, and has lived most of 
his life in London. Has been clever and industrious, and for eight years 
has been parliamentary reporter for the Standard . Always of a cheerful 
disposition, inclined to be erotic; never drank to excess. Had syphilis 
when 80 (history of chancre, &c.; has a penile scar); was treated only 
for a short time. Married w hen 31; had three children ; his wife had no 

Present illness .—Early in 1896 all his children died, and in March, 
1896, he was noticed to become very depressed, and would sit for hours 
brooding over his troubles, refusing to answer questions of his friends 
at all, or only answering them in monosyllables. A tremor of his hand, 
(considered to be writer’s cramp) was at this time noticed; his speech 
also became slow and hesitating, and his intellectual faculties noticeably 
impaired; but he showed no evidence of moral obliquity, nor did he 
exhibit any sign of exaltation. ThiB mental deterioration and depression 
steadily increased, and the tremor of his hand became more marked and 
his speech distinctly slurred, so that he was, in October, 1896, taken to 
St. Winifred’s Well for treatment, and while there, one night wandered 
from the hotel where he was staying and fell down a quarry, but sus¬ 
tained no more serious injury than resulted from spending a night in the 
open in the most inclement weather. From this time, however, he was 
observed to become rapidly worse, so that he was quite irrational, and 
developed well-marked delusions of grandeur. He was then, on October 
24, 1896, brought to this asylum. A well-marked Jewish type, with an 
expressionless, masked-like face. He showed much dementia; was unable 
to fix his attention, had lost all feelings of affection for his relations 
and friends, and had considerable loss of memory. He also exhibited 
extreme exaltation and grandiose delusions. Thus he was the “ King 
of England ” and “ Emperor of Germany,” possessed 150 gold mines, 
millions of money, and many valuable jewels. He stated that he was 
the strongest, cleverest, and richest man alive. Very egotistical, he was 


for ever boasting of his own prowess in various ways; he had well- 
marked bien etre . 

Obvious tremor of hands, face and tongue; reflexes much exag¬ 
gerated ; no ankle clonus. Pupils irregular, unequal, reacting slowly to 
accommodation but not to light. His speech was typically slurred and 
indistinct; his muscular power was poor; he was considerably wasted; 
Had shortening of left leg and anchylosis of hip from tubercular disease 
in childhood. 

Progress .—He became more demented and more feeble, and, though 
his appetite was good and latterly he took his food ravenously, he lost 
weight and became so weak that on November 25 he had to take to his 
bed. During this time, however, he never lost his exaltation, sense of 
bien Stre , or grandiose delusions. He gradually lapsed from a condition 
of gross dementia into a comatose state, in which he died on December 
14, 1897, much emaciated. He never had any seizures. 

Case 17. 

F. P., aged 43, married; a pensioner. 

Family history .—Mother in Gloucester Asylum. 

Personal history .—Was born in Gloucestershire, and has travelled 
much, having been in the Royal Navy all his life. Has been an un¬ 
commonly smart seaman, having seen a good deal of active service, having 
obtained several medals, holding a first-class gunnery certificate, and 
having been selected from a large number to be one of the gunnery team 
which performed at the Earl’s Court Naval Exhibition. Has had syphilis 
(scar on penis, scar in the groin, pigmented scar of ulcer on leg). Has 
not been a heavy drinker. Married when 28; two children alive, two 
dead. Always been of a cheerful disposition. 

Present illness .—In 1891 had a severe fall, and since that time has had 
fits, after which he would become very silly in his behaviour, and would 
often suffer from insomnia; these were supposed to be epileptic fits. He 
never complained of headache. 

Was admitted on July 9, 1897, grossly demented; he could answer 
none but the simplest questions intelligently; had marked loss of memory 
for remote and recent events, and had no idea of time and place; is 
dull, apathetic, and has no delusions or hallucinations; is not exalted. 
Is stated to have had aural and visual hallucinations at times. Urine 
1025, acid, no albumen, no sugar. Pulse 80, irregular, feeble. Pupils 
unequal (R. larger); react to accommodation but not to light. Hearing 
and sight fair. Feeble muscularly. Gait spastic ; reflexes much increased; 
ankle clonus present; marked tremor of face, tongue, and hands; arti¬ 
culation jerky, slurred and indistinct. Head measurement, C. 56, Ap. 84, 
Bp. 15, Bm. 14. Co-ordination bad ; constipated. 

Progress .—He became more demented and more feeble, so that before 
his death, on October 18, 1897, the degree of his dementia was such that 
he did not know his own name, while he was so feeble that he could not 
stand, and was confined to bed for forty-one days before his death on 



that account. He never had any seizures while here; he never com¬ 
plained of headache, nor did he ever exhibit any sign of exaltation or 
depression. He constantly was grinding his teeth together. 

Case 18. 

C. M., aged 87, married; a jeweller’s assistant. 

Family history.— His parents were cousins. His sister is of a nervous 
temperament, and at times very depressed. 

Personal history. —Was bom in London, and has always lived there 
or in other large towns. Has always followed the trade of a jeweller, 
and has apparently got on fairly well at it. Had influenza in 1895. 
Some years ago sustained a fracture of the skull (R. frontal region). 
Has been a heavy drinker; has had a good deal of domestic worry lately ; 
has had gonorrhcea four times; has had syphilis (history of), has now 
scar on groin. Married when 28; three children, one dead. 

Present illness. —For the last twelve months he has been unable to 
work; for eight months has been very reserved, but occasionally showed 
sudden fits of temper. When he first came under observation, August 16, 
1897, he was grossly demented, with marked impairment of memory for 
remote and recent events. He is childish, emotional, rambling, and 
incoherent; takes no notice of his surroundings; has a vacant expression ; 
masturbates. Urine 1020, no albumen, no sugar. Pulse 70, regular. 
Pupils unequal (R. larger); react slowly to light and accommodation. 
Hearing and sight fair. Touch impaired; marked tremor of hands and 
face; reflexes increased. Speech slurred, hesitating and tremulous. 
Considerable muscular weakness (he is hardly able to stand). TakeB his 
food indifferently; is thin; is constipated. Has a large depressed scar 
in frontal-region. Head measurement, C. 58J, Ab. 82}, Bp. 15}, Bm. 18. 

Progress. —From the time of his admission till that of his death, 
three months later, he got progressively worse, without even the most 
temporary improvement. At first there was considerable difficulty in 
getting him to take his food, owing largely to a delusion that it was 
poisoned. His dementia increased, so that for a month before his death 
he could not understand the simplest questions, and when asked his 
name would merely make an incoherent noise. Throughout his illness 
there was marked gastro-intestinal disturbance; his constipation was 
obstinate; his breath was very offensive, and at times he used to vomit. 
Emaciation was extreme before his death, which took place on November 
18, 1897. He never exhibited either exaltation or depression. He had 
a marked antipathy to wearing a hat, presumably owing to some de¬ 
lusion. He never had any seizures. He complained very frequently of 
severe headache, apparently frontal. Grinding of teeth noticed. 

Case 19. 

.T. B., aged 89, single ; a dock labourer. 

Family history. —Nothing known. 

Personal history. —Little is known of his history, except that he was 
in Leavesden Asylum in 1881. He was first admitted to Clay bury in 


May, 1896. His mother then stated that he had been queer for a long 
time, being obscene and liable to violent attacks of passion and used 
to threaten his relatives with violence. He was then considered to be 
suffering from congenital imbecility with mania. Impulsive, obscene in 
his language ; a persistent masturbator ; he was foolish in his behaviour 
and childish in his conversation. In January, 1897, though quite unim¬ 
proved. was taken away by his friends. States that he has had syphilis 
(has scars of former bubos in both groins). 

Present illness .—Was re-admitted on September 7, 1897, suffering 
from advanced general paralysis. Grossly demented; quite unable to 
give any account of himself; childish and incoherent, with great loss of 
memory for remote and recent events; he has marked bien etre and 
some exaltation with grandiose delusions. 

Urine 1080, acid, no albumen, no sugar. Pulse 112, small, regular. 
Pupils equal and regular; react slowly to both. Tremor of face. 
Reflexes increased. Co-ordination good. Speech slurred, tremulous and 
indistinct, with inability to say any long word. Dynamometer, R. 85, 
L. 90. Sight, touch and hearing fair. Double mitral murmur. Good 
appetite. No constipation. 

Progress .—He died on October 18, 1897, and during the short time 
that had elapsed since his admission showed no sign of improvement. 
On the 16th he had a seizure and never recovered consciousness, and 
subsequently was found to be hemi-paretic and to have slight broncho¬ 

Case 20. 

H. B., aged 40, married ; a messenger. 

Family history .—No definite history of insanity, but mother was 
always eccentric and especially so at the climacteric. 

Personal history .—Born in London and has lived there most of his 
life. Got on moderately well at school and went to work when 16; he 
always bore a good character and was steady and considered to be a 
smart salesman. He has been of a bright, cheerful and affectionate 
disposition. Was never in the army. Married when 27 ; four children 
alive, one died at six months from congestion of the brain. His wife has 
had no miscarriages. He has suffered from tonsillitis and rheumatism. 
Never drank to excess. Has a penile scar. 

Present illness .—Twelve months before admission his eyesight began 
to trouble him. He attended Moorfields Hospital, where they diagnosed 
“ primary atrophy ” of early tabes. Then his vision was R., L.; 
pupils were unequal (L. larger), reacting to accommodation but not to 
light; he had “ pricking and shooting pains in the eyes and saw double 
both discs were pale with small arteries and large veins; the fields of 
visions were contracted and more so in the right than left eye ; he had 
no knee-jerks and frequent micturition; he was treated by mercurial 
inunction. Seven months ago, owing to his eyesight becoming worse, he 
had to give up his work and about this time became depressed, but soon 
developed delusions of a grandiose nature, such as that he had a lot 



of money; he would lay plans of an extravagant nature, in order, he 
said, to benefit his children in the future. At this period he seems 
to have exhibited marked dementia, as he would wander about the streets 
in an aimless manner, unable to find his way home. His moral sense 
does not seem to have been in any way blunted. His speech was 
affected; his hands and lips were noticed to be tremulous and he lost 
weight, although he had a 44 wonderful appetite and could eat almost any¬ 
thing.” He was admitted on July 8, 1897, showing much loss of 
memory, giving a most incoherent account of himself and presenting 
other signs of dementia. At the same time he was exalted and had 
delusions of grandeur, such as that he had a title, .£50,000 and was 
immensely strong. His bien itre was obvious. 

Urine 1020, acid, no albumen. Pulse 64 , regular in force and 
frequency, readily compressible. Tongue fissured, with small ulcer 
on right edge ; palate high; appetite good; teeth fairly good. He was 
constipated. He was thin ; had pigmented spots on the back, abdomen 
and arms; had a small sore on the inside of his foot. His sight was 
impaired. Touch and hearing good. Pupils unequal (R. larger); react 
badly to light and accommodation. Muscles soft and flabby. Dynamo¬ 
meter, R. 80, L. 80. Co-ordination impaired; knee-reflexes absent; 
marked tremor of tongue and face, slight of fingers. Speech slurred. 
Head measurement, C. 55, Ap. 87, Bp. 15, Bm. 14. 

Progress .—Shortly after admission he had retention of urine, which 
was due to atony of bladder and not to any obstruction of the outlet. 
This improved under strychnia. The progress of his disease w as marked 
by a steady increase of dementia till it became so gross that he gradually 
ceased to formulate delusions, and latterly could not even tell you his 
name. Physically, notwithstanding his ravenous appetite, he became 
much emaciated and so weak that he could not stand. He died on 
December 22, 1897. 

Case 21. 

F. M., aged 88, married ; a coachbuilder. 

Family history .—There is no history of insanity, phthisis, or drink 
in the family. 

Personal history .—Born and always lived at Merton. Got on fairly 
well at school; went to work as a carrier’s boy when 10, and at 18 was 
apprenticed to a coachbuilder, and has always worked at that trade since. 
Married when 28, has five children alive, one died (cause unknown). 
Never had any serious illness. Of a fairly cheerful temperament; never 
been a heavy drinker. Has been of an erotic disposition. 

Present illness .—September, 1896, failed in business, and got into 
straitened circumstances; became depressed and refused food; then he 
would become very excited at times, and suffered from insomnia; and 
was admitted on July 5, 1897. He then exhibited great mental exalta¬ 
tion, considering that he was a wonderful singer, was the best bicycle 
rider in the world, intends building a large house, and, indeed, considers 
that he and all connected with him are very wonderful persons. He is 


intensely egotistical, gabbling about what he has done, and still more 
about what*he is going to do; he is excitable, unduly emotional, and has 
well-marked bien Hre; he shows only a very slight degree of dementia. 

Urine 1020 acid, no albumen. Pulse 84, regular, good volume. 
Tongue clean and tremulous; bowels regular; appetite good. Has a 
mitral systolic murmur. Sight, R. g, L. g. Hearing and touch good. 
Co-ordination good. Speech slightly slurred. Muscular power good. 
Dynamometer, R. 120, L. 125. Slight tremor of face and hands. Re¬ 
flexes exaggerated and wrist-jerk present. Pupils are equal, regular, 
react fairly well to light and accommodation. 

Progress. —Unfortunately, he only remained in this asylum till 
October 29, during which time he remained in much the same condition, 
deteriorating both mentally and physically at a very slow rate. He 
never had any seizure. I learn, however, that he is becoming weaker 
and losing weight, and is more demented than he was. 

Case 22. 

T. S., aged 81, married ; labourer. 

Family history. —There is no history of insanity, alcoholism, or 
phthisis in the family. 

Personal history. —Got on well at school. When 12 went on board a 
training ship, and left that to go as a packer at Waterlow k Sons ; when 
19 he went into the army, but has never been further from home than 
Ireland; he served seven years. Married when 27, and had three chil¬ 
dren who are all living; his wife has not had a miscarriage. He denies 
ever having had syphilis or other venereal disease. At times he has 
drunk heavily. He was erotic. 

Present illness. —About the beginning of 1894 a change was noticed in 
his manner; he was very irritable and bad-tempered, would talk in a 
very excited way, and threatened to commit suicide; he suffered from 
insomnia; at times he would leave home for weeks together. He w as 
in great poverty during this time. He was admitted in April, 1897; he 
then showed a considerable degree of dementia, and made long, rambling, 
and incoherent statements about himself, exhibiting marked egotism 
and some exaltation. His memory is poor, especially for remote events, 
and his reaction to questions slow. On the whole, he is good-natured 
and has a sense of bein itre. He is excitable. 

Urine 1029, acid, no albumen, no sugar. Pulse 80; vision, $ both 
eyes; hearing and touch good. His appetite good. His bowels regular. 
Pupils unequal (left larger), react fairly to both. Fundus oculi normal. 
Co-ordination fair; muscular power fair. Marked tremor of hands, face 
and tongue. Reflexes exaggerated; speech indistinct, slurred, and 
tremulous. Head measurement, C. 55$, Ap. 81$, Bp. 15, Bm. 18$. 

Progress. —At first he was rather excited, inclined to be aggressive, 
but soon became quieter; and as he became more demented, gradually 
lost mental power to do more than just answer his name ; at the same 
time he lost weight, and his speech became worse. He died on June 20, 



1898, having for the last month of his life lost weight and mental power 
rapidly; and during the last three days had a succession of slight 

Case 28. 

J. A. D., aged 45, married; labourer. 

Family history .—There is no history of insanity, alcoholism, or 
phthisis in the family. 

Personal history .—Bom at Woolwich, and has lived in a variety of 
places in England and Ireland, and also served in the army abroad 
(Gibraltar, Malta, India); he went to work when 15 in the shop of a 
mathematical instrument maker. Has always been rather a reserved 
man. He had an injury to the head when 88, and another when 40, 
when he appears to have sustained a fracture of the skull from bricks 
falling. Married when 28; has had no children. Has never been a 
heavy drinker. 

Present illness .—Strange in his manner since 1895, being always very 
sleepy and having no life in him; difficulty in walking has also been 
noticed for some time past. He was admitted on September 11, 1897, 
mentally grossly demented, being unable to give his history, having a 
bad memory for remote and recent events ; when asked questions, giving 
incoherent answers, apparently answering his own thoughts rather than 
the questions asked. He is exalted, egotistical, and has a sense of 
bein etre ; but his dulness, apathy, and intellectual bluntness overshadows 
everything else in his mental condition. 

Urine 1080, acid, no albumen, no sugar. Pulse 100, small, regular. 
Pupils unequal, irregular, act badly to both light and accommodation; 
slight B. ptosis. Sight, hearing and touch fairly acute. Bedexes are 
diminished; co-ordination fairly good. Tremor of face marked, and of 
hands slight. Dynamometer (grasp), B. 75, L. 65. No cardiac or 
visceral disease detected. Speech markedly slurred. He is thin; ap¬ 
petite good. 

Progress .—He died on November 25, 1897, the only change which 
took place in his condition being an increase of his dementia and a loss 
of weight. He had several seizures shortly before death ; during these 
his temperature rose to 105°. 

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BY F. W. MOTT, M.D., F.B.S. 

Prior to 1877 general paralysis of the insane was 
believed to be essentially a disease of adult life only. In 
that year Professor Clouston described a case of the disease 
in a boy, aged 16, and he pointed out that clinically and 
pathologically the disease that affected his patient in no 
way differed essentially from the adult form ; he termed 
it developmental general paralysis, and it was looked upon 
by him as an extremely rare condition. Since his discovery, 
cases have been published in various lands, and as the know¬ 
ledge of the existence of this disease has become dissemi¬ 
nated, so the number of cases has increased, and I myself 
have been able to collect the notes of twenty-two cases 
occurring in the London County asylums during the last 
three years. Eighteen of these cases I have myself seen, 
and I have no doubt that a few cases have been overlooked 
and that this number does not represent all the cases. In 
1895, Alzheimer, in a very valuable paper, collected and 
analysed thirty-seven published cases and added three cases 
of his own, with careful microscopical examinations of the 
nervous tissues. In 1898, Thiry collected and analysed 
sixty-nine published cases, which include all those of 
Alzheimer with three cases from the clinic of Haushalter, 
which he has investigated. Both these authors come to the 
conclusion that syphilis plays a predominant role in the 
etiology of the disease. 

Dr. Purves Stewart has recently published in Brain 
three cases, in one of which there was a post-mortem. 
These are not included in Thiry’s statistics, so that the 
recorded cases with post-mortem examination will very soon 
reach three figures (72 4- 1 + 16 = 89). 


The cases which I have collected are not so numerous as 
those collected by Alzheimer and Thiry, but they have the 
advantage in one way of being derived from the same race 
and locality; moreover, I have myself seen most of the 
cases, and examined the majority clinically and patho¬ 
logically. The results, however, agree strikingly in the 
main with the deductions made by these two observers in 
their valuable monographs, and an attempt will be made to 
compare my own conclusions with the conclusions of these 
authors. It was my intention to analyse all the previously 
recorded cases, but this work has been so admirably com¬ 
pleted quite recently by Thiry, that I shall make free use of 
his analyses and observations. 


The number of cases recorded increases every year, and, 
although the disease is rare, it is, for reasons previously stated, 
not very rare. Thiry remarks that at the clinic of Professor 
Haushalter, out of 7,000 children whom he saw in four 
years, general paralysis was found in three cases only. No 
doubt a great many cases would be overlooked. The case 
H. I., which I saw as an out-patient at Charing Cross 
Hospital, before I had experience of asylum practice was 
not recognised by me as a case of general paralysis. 

Thiby’s Collected Cases. Mott’s County of London Cases. 

Age of Onset. 


case at 

.. 8 


1 case at 

.. . . 8 years. 



.. 9 



.. .. 12 „ 



.. 10 



.. .. 14 „ 



.. 11 



.. .. 15 „ 


• 1 

.. 12 



.. .. 16 „ 



.. 12 



. 17 „ 



.. 13 



.. .. 18 „ 



.. 14 



.. .. 19 „ 



.. 15 



.. .. 20 „ 



.. 16 






... 17 


Total 16 cases 

Average 16 years. 



.. 18 


3 ii 

.... 21 „ 



.. 19 


1 „ 

.. .. 22 „ 



.. 20 


2 „ 

.. .. 23 „ 

Total 68 cases Average 14 years. Total 22 cases Average 17 years. 



The difference in these statistics as regards age is 
probably owing to the fact that Thiry’s are based upon 
recorded cases, and only those would be recorded which 
occurred in very young people, and were therefore deemed 
interesting. I have, on the other hand, recorded all the 
cases which I could find during the last three years in the 
London County asylums, even up to 23 years, which makes 
the average of time of onset, of course, higher than Thiry’s. 
In fact, as Case 4 F., p. 306 shows, probably congenital 
syphilis may, with an exciting cause, give rise to general 
paralysis at any age, provided the exciting cause arises. 

Thiry concludes that it is probable that in well-prepared 
statistics the number of cases of juvenile paralysis would go 
on increasing up to 20 years, the maximum being at 19, 
and he believes that general paralysis does not habitually 
coincide with the development of puberty. According to 
Clouston and other authors who have written upon this 
subject, it is concluded that the sexual crisis is an exciting 
cause in the development of this disease. Saiki writes: 
“ Contrary to other diseases of youth which begin at the 
end of puberty, juvenile general paralysis begins generally 
at the age of 13 to 15, the commencement of puberty, of 
which it stops the evolution and it thus plays the role of 
exciting cause, the true causes being reserved for neuro¬ 
pathic heredity and to hereditary or acquired syphilis.” 

In my opinion there may be many exciting causes, and 
nearly always the predisposing cause to the disease is 
hereditary syphilis. 


In the adult form men are much more frequently attacked 
than women, but in the juvenile form, as my statistics 
show, the sexes are equally affected ; moreover, as Thiry 
points out, if a sufficiently large number of recorded cases 
be collected (as he did) the sexes will be seen to be equally 

Wigglesworbh found in his statistics five males for eight 
females, and he concluded that it was commoner in females, but 
when these are added to the statistics of other observers, it will 


be found that out of sixty-two recorded cases in which the sex is 
given, there were thirty males and thirty-two females. 

As a rule, the females were older on admission to the 
asylum and at death than the males, and as in the adult 
form it seems to run on an average a more rapid course in 
males (about two years’ duration in asylum and in females 
about three years), so apparently it does in the juvenile form. 

In the female cases which began either at or before 
puberty, menstruation never came on, or if it did, it soon 

Dr. Helen Boyle recently read before the Medico-Psycho¬ 
logical Association the account of C. V., Case 2. She assumed 
that syphilis was absent in this case. I think reference to 
the notes shows that, although it is not proved, it certainly 
cannot be excluded. She also alluded to the fact that menstrua¬ 
tion bad never come on and therefore it might be that the brain 
disease was due to a failure on the part of the reproductive 
organs to produce an internal secretion. In some cases, how¬ 
ever, menstruation does come on at puberty and then ceases. 

When the disease occurs at or before puberty there is 
usually infantile development of the reproductive organs. 
This was strikingly shown in Cases 1 and 3 F. and Cases 2 
and 4 M. It is possible that masturbation may play some 
part in the more rapid progress of the disease in males. 

Social Condition. 

All the cases were from the lower or lower middle 
classes. Six of the eleven females were able to earn their 
living for a time. Five were unable from mental deficiency 
or the early onset of the disease to take up an occupation. 
Amongst the males, seven were able to work and four were 
not. Some few were above the average in intelligence 
before the disease came on (F. A., Case 5 ; M. G., Case 10; 
P. C., Case 11). Several were congenitally deficient 
imbeciles, e.g., H. I., Case 4, and E. E. G., Case 1. 

Exciting Causes. 

Several males and females first showed signs of the 
disease about the period of puberty. In one case the puer¬ 
peral condition and desertion was clearly the exciting 



cause (M. W., Case 4). One case seemed to follow a fall 
from a van ; both of these cases, however, had definite 
congenital syphilis. In several of the remaining cases 
worry was the cause assigned and in one masturbation. 

Hereditary Insanity or Neuropathy. 

In three of the male cases the fathers suffered with 
general paralysis, and, although in not one of these men 
was there definite evidence of syphilitic residua, yet their 
offspring in two cases, A. E. and A. B., showed definite 
signs of congenital syphilis, and the maternal history of 
miscarriages and still-births in the other case, A. H. B., 
made it practically certain. In A. B. there was a history of 
collateral insanity. We must, therefore, consider that 
hereditary insanity in these three cases played a far less 
important part than the syphilis which the fathers acquired 
and transmitted to their offspring. The notes expressly 
state that there was no hereditary taint of insanity in twelve 
cases. There was direct insanity in three cases and in 
three collateral insanity. 

I do not agree with Thiry, therefore, in assuming that 
hereditary neuropathy is a very prominent factor in the 
production of this disease. 

Infectious Diseases. 

It is conceivable that measles, influenza, scarlet fever 
and other infectious maladies might predispose to the dis¬ 
ease, but all the evidence points to one specific infection— 
syphilis—as the cause above all others which produces this 
early degeneration of the nervous system. 

In none of the twenty-two cases recorded can syphilis be 
excluded. Thirteen showed definite signs upon the body, 
and I cannot, therefore, agree with Dr. Purves Stewart 
when he says that it is rare to find such. Of the remaining 
eight cases the history was doubtful in several, viz., 
Cases 6, 7, 8, F. and 8 M., but in not one of these 
cases could syphilis be excluded. In the remaining four 
cases, although there were no signs on the body, there 
was a definite maternal history of miscarriages, still- 


births, &c., and in one case, 3 F., the mother had had signs 
of infection, and a sister had keratitis and syphilitic teeth. 
There is reason to believe, therefore, that there was 
probably a syphilitic origin in all of these cases, although 
there are only proofs on the body of 60 per cent., and 
if combined with maternal history of 80 per cent. It is 
possible, however, that some cases were overlooked be¬ 
cause they had not signs of syphilis on the body. It is 
remarkable how seldom one found the mothers of syphilitic 
children suffering with any signs of the disease themselves. 
Most of those whom I interviewed gave no history of syphilitic 
disease, yet their children had all the signs of congenital 
syphilis. We may suppose that in some of these cases the 
infection was only spermatic; possibly the mother obtained 
an immunity to the disease by absorption of the toxin 
from the developing syphilitic embryo in graduated doses. 
B. L., Case 2 M., was an instance, however, where the 
mother was suffering with definite syphilitic symptoms, for 
just about the time of his birth she became blind; again, 
the mother of E. B., Case 3 F., had signs of syphilis after 
marriage. The maternal history in a number of the cases 
is instructive in showing the fatal effects of syphilis on 
infant life, and therefore upon the birth rate—a fact of 
vital importance to the country. Thiry, in the analysis of 
his sixty-seven cases, found syphilis in G4 per cent., a figure 
which he says is too great to assign to this infection only a 
secondary role in the genesis of the disease; but in the 
remaining twenty-four cases, where it has not been recorded, 
one can nevertheless suspect it by reason of the history. 
There were few of his cases only iu which it could be 

Duration of the Disease. 

Of those that have died (males seven) there were two 
which lasted only 3 months, two 18 months, one 1 year, and 
one 7 years. Among the females the shortest was 6 weeks 
but death was caused by complications, and the longest was 
7 years. The cases which begin young seem, as a rule, to 
last longer; those which begin at 20 or after, last a very 
short time, and take on the acute galloping form of the 



disease. In women the disease is frequently complicated 
with phthisis. As a rule, the male cases seem to run a more 
rapid course than the female. 

Mental Symptoms. 

In many of these cases the patients were mentally de¬ 
ficient from birth; in others there was a period of gradual 
mental enfeeblement coming on in a young person who was 
fairly healthy and had an occupation. In fact, it is very 
difficult to determine when the disease began in some of the 
cases; in some, however, we can make a pretty certain guess 
by the fact that they would not be employed long after they 
had shown signs of mental degradation. For example, 
A. J. R., who was in the Royal Navy, would not have been 
sent out in a battleship to the Mediterranean last year if he 
had had fits or shown any definite signs of insanity. 

In all cases there was progressive dementia. That was a 
constant mental symptom. Some patients previously in¬ 
telligent became dull and progressively enfeebled mentally, 
until actual dementia set in. In three cases the mental 
symptoms at first noted were like those of acute mania. 
Other cases and more numerous, began with mental de¬ 
pression, sometimes with delusions of persecution. Delu¬ 
sions of grandeur were not nearly so common as in the adult 
form, but they occurred in several cases. 

Motor Symptoms. 

Progressive paresis is noted in every case, except one, 5 F. 
Paralysis and contracture of the lower limbs, occurred in 
quite half the cases. Tremor of the face muscles, tremulous 
tongue, and slurred speech, together with affection of the 
handwriting were noted in all the cases which I have 
personally observed. In many of the cases, especially those 
of some duration, speech became entirely lost, and often 
there was difficulty in swallowing. Frequently there was a 
curious smacking of the lips, champing and grinding the 
teeth. Ataxia was noted in one case, and the first symptoms 
were lightning pains in the limbs (5 M.). 

The knee-jerks were absent in four cases, exaggerated in 
the great majority of the rest. 


In one case the condition of the pupils was not noted. 
In the remaining twenty-one cases there was pupilary 
affection. In thirteen the pupils were unequal. In nine they 
are noted as irregular. In all those noted (twenty-one) the 
reaction to light is stated to be sluggish or inactive. In 
some accommodation is also affected. 

Undersized, ill-developed bodily condition is the rule. In 
several of the cases of either sex the reproductive organs 
were of infantile development, and there was absence or 
scanty development of hair on the pubes. It will thus be 
observed, that the symptoms and progress of this early form 
of the disease differ but slightly from those met with in the 
adult form. I think the most important difference which 
I could observe is, as a rule, the mild form of convulsions 
when they occur, and the comparative infrequence of delu¬ 
sions of grandeur, but the important cardinal symptoms of 
the disease in the adult form are present also in the juvenile 
form, namely, progressive dementia, progressive paresis, affec¬ 
tion of verbal and written speech, pupil phenomena, altered 

Pathological Anatomy. 

In sixteen cases post-mortem examinations have been 
made and the characteristic naked-eye lesions of general 
paralysis found. In eight microscopical examination of 
tissues was made. In all cases the change was essentially 
the same as that met with in the adult form of the disease, 
and I did not find any case showing the changes described 
by Alzheimer, as occurring in one of his three cases ; for I did 
not find mastzellen nor atrophy of the cells of the 3rd and 
4th layers, while the superficial layers escaped. In six cases 
where the two halves of the brain were weighed, the left 
hemisphere weighed less than the right, as follows :— 


Case 7 F. =360 



„ 9 F. = 420 

. . 

. . 


„ 8 F. = 438 

. , 

. . 


„ 1 F. = 417 

. . 

. . 


7 M. = 520 

. . 

. . 


„ 3 F. = 346 

. . 

. . 


Speech was markedly affected in all these cases. 

Average difference in favour of the right hemisphere = 28 grammes. 




Atrophy of the brain, especially the frontal and central 
convolutions, and thickening of the pia-arachnoid membranes, 
dilatation of the ventricles and granular ependyma were 
found in all the cases examined. The unequal weights of 
the two hemispheres is of very considerable interest, seeing 
how profoundly speech was affected in these cases, especially 
1 and 3 F., in which it was entirely lost. Microscopical 
examination of the brain showed the same lesions as in 
the adult form of the disease, viz., atrophy of the tangential 
fibres, atrophy and disintegration of the neurons of the 
cortex, especially of the frontal and central convolutions, 
the occipital being comparatively but slightly or little 
affected (see page 276 and photomicrograph). There is 
usually a marked overgrowth of glia cells and a cellular 
proliferation around the vessels. For further particulars 
concerning the changes met with see microscopical ex¬ 
amination in Cases 1, 3, 7, 8, 10, F. and 4, 5, 7, M. 

It will be observed that in four of the cases examined 
there was syphilitic pericellular and perivascular fibrosis of 
the liver. 

As, probably, I shall have the opportunity at some future 
period of examining the tissues of the cases which are still 
under observation, I shall leave to a future number of the 
Archives a fuller summary of the pathological anatomy of 
this disease. 

Remarks upon Diagnosis. 

In the selection of these cases, amongst the large number 
of inmates of the London County Asylums, I have met with 
difficulties in diagnosis, especially in the early stages of the 
disease; and my experience may be of some use to my 
readers. I may, however, say that I have never once been 
deceived in the diagnosis, for post-mortem results have 
verified in every case the opinion which I formed during life. 

As we have observed in the study of these cases, there 
seem to be two types of the disease, one in which a mentally 
deficient child or a congenital imbecile suffering with fits at 
some period, varying from the age of eight years onwards, 
develops new symptoms of mental trouble which become 


progressively worse and are associated with progressive 
motor failure, invariably affecting the speech, the pupils 
and the knee-jerks, and lasting a variable time. As a rule, 
the duration of the disease in these cases shows that it 
was longer when it commenced at an early age. The other 
type is when a normal child, even a bright, intelligent child , 
about the age of puberty, or even at any time afterwards up 
to one or two and twenty, becomes affected mentally and 
shows a gradual progessive dementia and paresis. This is 
true only to a certain extent, for it is probable that had we 
been able to study the patient in whom the disease had run 
apparently a much shorter course, we should have discovered 
some mental symptoms earlier. 

A short time ago there were at Colney Hatch twenty 
cases of mentally afflicted boys and youths; among these 
there were no juvenile general paralytics as far as I could 
ascertain ; some were congenitally deficient mentally, some 
were afflicted with epilepsy, and not a few were imbecile 
epileptics. The epilepsy in some of the cases was probably 
due to organic brain disease, such as tumours, specially 
tubercular, some to probable birth-injuries. Two only of 
these twenty cases showed well-marked signs of congenital 
syphilis, a much lower proportion, as will be observed, than 
in the twenty-two cases of juvenile general paralysis which 
are here recorded. One case may develop into juvenile 
general paralysis, for he is only 11 years of age ; he had 
typical Hutchinson’s teeth, linear cicatrices around the 
mouth, chorio-retinitis, unequal pupils, infantile development 
of reproductive organs, retained testicle ; hut the mental 
symptoms pointed to moral insanity, he was wilful, danger¬ 
ous, and unmanageable by his parents. Latterly, owing 
partially to keratitis and partly to optic atrophy, his sight 
became much affected, but I have come to the conclusion 
that he is not a case of general paralysis, for he was un¬ 
usually sharp, and showed no signs of progressive dementia, 
nor did his speech become affected, nor did he have any 
fits. He has lately been discharged. 

The other case is one which is recorded as showing the 
effects of congenital syphilis in the production of congenital 



imbecility and epilepsy, and these cases are not at .all 
infrequently met with (p. 266). Very possibly the fact of 
their being put into an asylum early removes the exciting 
causes which might lead to the acute process of decay 
coming on. This is strikingly shown in the history of 
A. J. E. (p. 282). There were three brothers, all with signs 
of congenital syphilis; one, in the Koyal Navy, up till 20 a 
comparatively healthy individual, but breaks down and dies 
of acute general paralysis in three months; his younger 
brother, a congenitally deficient imbecile with more marked 
signs of syphilis on the body, is sent into Caterham Asylum 
at 16 years of age, and so far presents no signs of acute 
degenerative processes occurring. It is conceivable to 
believe that had this lad been under the same conditions 
of stress as his brother, namely, in a man-of-war just on the 
verge of war breaking out, the acute process would have 
been set up. Again, the case 59 (p. 162) is a remarkable 
one as showing the slow form of mental decay which con¬ 
genital syphilis will produce, terminating in absolute im¬ 
becility. The history of the family in that case is also 
of great interest as exhibiting the direful effects of syphilis, 
killing the husband and the wife and causing imbecility in 
two of the children and some mental degeneration in the 
other two. 

However, with regard to diagnosis, although we know 
that syphilis is likely to produce congenital imbecility and 
epilepsy, still the proportion of these cases due to hereditary 
syphilis is far less than those of juvenile general paralysis. 
By this I mean that twenty-two cases of congenital imbe¬ 
cility or that with epilepsy would not yield anything like a 
history of 80 per cent, hereditary syphilis. Therefore, a 
history of congenital syphilis, and especially combined with 
signs on the body, occurring in a young person who shows 
about the time of puberty or afterwards signs of mental 
decay which were not previously present, should always 
make us suspect this disease. A great deal of importance 
has been attached by some authors to hereditary insanity 
in the family, direct or collateral; my experience seems to 
show that this is not of so much importance, a history of 


alcoholism in the parents is quite as frequently met with. 
These cases of general paralysis, arising in the subjects of 
hereditary syphilis, are of very great interest from this point 
of view. At what age may the symptoms develop ? There 
is no precise period. If we consider that the pathology is 
one of diminished specific vital energy of the neurons, then 
they will not undergo decay until the other essential factor, 
stress , occurs. An interesting example of this is shown in a 
case, p. 306, where pregnancy and desertion occasioned the 
onset of a rapid process of decay of the brain. This might 
have occurred at a later period, and it seems to me a feasible 
argument that some of those adult cases in which acquired 
syphilis can be excluded and the disease comes on, may be 
due to the fact of inherited syphilis. But this argument 
is not proven. I have just recently seen a case bearing on 
this subject which I will briefly record. 

H. T. A., female, aged 24, admitted to Cane Hill Asylum. Diagnosis 
general paralysis. Married four years last Christmas. First baby born 
dead; second, girl, is alive, aged 1 year. She did not suckle the baby 
after three months. Was admitted February 10, 1899. For six weeks 
previously she had been suffering with progressive mental failure and 
lots of memory. She has much improved since she has been at the 
asylum, now four months. Is well nourished, good colour, short and 
stout, and very anxious to go home. The doctors in charge hesitate 
to accede to the wishes of her husband, fearing that she will break 
down again. 

Physical condition .—She has three well-marked linear scars extend¬ 
ing from the left angle of the mouth, and several smaller ones at the 
right angle. There are two scars under the left chin, she says they are 
all from birth. The upper central incisors, especially the left, is peg¬ 
shaped and notched ; there is a very high-arched V-Bhaped palate. The 
tongue is tremulous, the speech is nasal and there is a slight tremor in 
the lips when she speaks. The hands are blue, indicating vaso-motor 
constriction ; the knee-jerks are absent, as she walks the heels come 
down first, and when she stands with her eyes shut she sways a little 
She complains of no pains in the legs, and the pupils are equal and 
react to light and accommodation. 

Mental condition. —She talks quite rationally, has no discoverable 
delusions, nor loss of orientation. She can multiply figures and shows 
no embarrassment on reversing the sum, 4 x 12 = 48, 12 x 4 = 48. 
Her husband states that she is now as well as ever she was, and he 
assures me that he never could have had any veneral disease. 

The practical question arises, should this patient be discharged ? The 
answer depends upon the following considerations. If it be a case of 



lactational neurasthenia in a congenital syphilitic, she may, under the 
stress of child-bearing and the worries of a home, develop general 
paralysis if she be not already in the initial stage. The doctors in 
charge were not, however, only influenced in their minds in discharging 
her, on this account, as on the probability that she would give birth 
to children mentally afflicted. It is very difficult to decide whether one 
ought to retain a patient who is apparently sane against her wish, and 
that of her husband, for possibly it is more likely to give rise to mental 
stress and worry than even the trials and troubles of a family and 
home. With regard to the second condition, the danger of inherited 
insanity is far less than in cases of non-organic origin. Moreover, 
advice might be given to the husband not to have children until his 
wife is entirely sound. 

I hope to interview the mother of the patient to find out further 

The fact that pregnancy and lactation may act as im¬ 
portant exciting causes in developing disease I have seen 
strikingly shown in the very recent development of tabes in 
a woman following pregnancy. The case ran a short rapid 
course. Again it is the experience of ophthalmic surgeons 
that keratitis is very liable to be developed in women suffer¬ 
ing with congenital or acquired syphilis after pregnancy. 
Sometimes cases occur in which the symptoms point at first 
simply to a functional disorder—mental depression; and 
Case E. M., p. 314, was admitted to Colney Hatch and 
certified first as mania, from which she improved so far as to 
be discharged. She returned again with signs of mental 
depression; she was again discharged; upon re-admission 
later on, the case was recognised as one of general paralysis. 
It is possible that even in the first instance there were 
symptoms which might have led the medical officers to 
diagnose general paralysis, but the rarity of this disease may 
have put them off their guard. Moreover, this young girl 
exhibited grandiose delusions in the first instance, a con¬ 
dition which is extremely rare in juvenile general paralysis. 

The case of A. B., already referred to, was diagnosed as 
epilepsy and imbecility, but when I heard the history of 
the man having been in the navy for eight years, of his 
having had symptoms only three months, that the fits were 
unilateral, that his speech was affected, and that he was 
demented, I came to the conclusion before examining the 
body (for I did not see him during life), that it was a case 
of general paralysis. 


Early cases of the adult form of general paralysis occur. 
I have met with cases in which the disease has come on at 
23 and at 24 years of age e.g., in the two following, with 
signs of acquired syphilis. 

(1) S. G. T., aged 28, admitted to Claybury, March 28,1895. She had 
pigmented syphilitic scars on back and on abdomen, and the typical 
signs of general paralysis ; namely, dementia, grandiose delusions, 
tremulous tongue, slurred and tremulous speech, exaggerated knee-jerks 
and paresis; the symptoms progressed, and she died eighteen months 
later. Post mortem, the typical lesions of general paralysis were found 
with acute phthisis. 

(2) W. L., aged 24, bookmaker; history of syphilis four years pre¬ 
viously, scar on penis, squamous syphilide on the body, enlarged 
glands. This patient presented all the characteristic signs of general 
paralysis, namely, progressive paresis, progressive dementia, slurred 
speech, muscular tremors, unequal sluggish pupils, tremulous and 
incoherent writing, exaggerated knee-jerks. The disease has progressed 
during the last two years, and he is rapidly getting into the third stage. 

As a rule the time which elapses between syphilitic 
infection and the origin of the disease is much longer than 
could have been the case in these two individuals, and it 
might be urged with reason by those authorities who con¬ 
sider that syphilis has nothing to do with general paralysis, 
that the existence of the signs of the disease on the body 
was a mere coincidence and had no causal relation to the 
organic brain disease. 

The fact that obvious syphilitic arteritis was not found 
in these cases supports the view of Fournier that the disease 
is parasyphilitic or metasyphilitic, as Mobius calls it. Ic is 
a premature decay, a degenerative process, like the decay 
and malformations of the teeth. These are developed out 
of the enamel germs; the cells which form the permanent 
teeth are present in the cavities of reserve at birth, so also are 
all the cells which will form the complex neurons. The 
life-history of those cells will depend upon the specific vital 
energy which they receive from the germinal plasm out of 
which they are developed. Some have not sufficient vitality 
to develop at all—hence when the permanent teeth are cut, 
erosions on the enamel and malformations mark the destruc¬ 
tive process which took place in the enamel germ. This 



applies to some of those congenital syphilitics who have the 
characteristic teeth, and a simile may be drawn to those 
congenital syphilitic children in whom idiocy and imbecility 
mark either premature death or arrest of the development of 
the higher and more complex neurons. Undoubtedly many 
congenital syphilitics are imbecile without obvious vascular 
lesions to account for the arrest of development. 

There is, however, this other condition in which the 
effect of the poison is manifested by defective vitality to 
resist stress, so that at puberty or adolescence the destruc¬ 
tive process of the nervous system begins and progresses. 
Here the whole neiVous system has been developed perfectly, 
but the physiological margin between repair and waste is 
narrow, and the equilibrium between the two, which should 
allow the nervous system to adapt itself to its surroundings, 
is under the influence of a number of factors which may be 
summed up as stress overturned. Of course in such a con¬ 
dition of things the hereditary factor, which may be either 
immediate or remote, must play a part, although it appar¬ 
ently is not of such great importance as in other forms of 

The following diseases might also be mistaken for the 
juvenile form of general paralysis juBt as they might for the 
adult form:— 

(1) Tumor cerebri .—The general symptoms of tumour, 
namely, vomiting, severe headache, and optic neuritis, are, 
however, absent in this disease, and although in some cases 
of tumour there may be dementia, unequal pupils, epilepti¬ 
form seizures, affection of speech and paralysis, yet the 
dementia is not so progressive, the pupils, although unequal, 
are usually not sluggish and inactive to light; reacting to 
accommodation. The epileptiform seizures are Jacksonian 
in type, and have a definite onset and march; the motor 
symptoms, whether they affect the speech, the face or the 
limbs, are paralytic rather than paretic, and are not asso¬ 
ciated with fine tremors. The lesion is coarse and local 
in tumour, and accordingly the symptoms are coarse, and 
local rather than diffuse and generalised as in general 


(2) Syphilitic brain disease. —A history of syphilis is a 
very important element in the diagnosis of juvenile general 
paralysis. If a young patient with signs of congenital 
syphilis and mentally affected comes under observation, we 
may have to decide whether the case is one of general 
paralysis or syphilitic brain disease. We must be guided 
by exactly the same rules as in the adult forms of the disease 
(vide p. 45). 

(3) Multiple sclerosis. —Perhaps more difficulty in making 
a diagnosis arises in regard to this disease than any other, 
especially when the patient is a young woman. Congenital 
syphilis is not usually met with in disseminated sclerosis ; 
the Argyll Robertson pupil does not occur; changes in the 
fundus oculi are not uncommon; in general paralysis the 
only changes that are found are grey atrophy of the disc 
and chorio-retinitis. Nystagmus is frequent, whereas I did 
not meet with it once in general paralysis. Symptoms 
often come on suddenly, and then there is a remission 
for a time. There is intentional tremor, but it is as a 
rule coarser, and affects the large muscles of the limbs; 
the speech is affected, but it is scanning rather than 
hesitant, syllabic and tremulous. The knee jerks are 
exaggerated; there is usually clonus, easily obtained. 
This latter is more marked, as a rule, than in general 
paralysis. The expression of bien etre or Vair de beatitude 
of Charcot gives a superficial resemblance to juvenile 
paralysis, especially when combined with dementia. But 
the mental symptoms are not so intense, nor is the de¬ 
mentia so steadily progressive and profound; the paralyses 
are coarser and more variable; there is not a progressive 
paresis indicating a generalised decay of the neurons, but 
the symptoms rather point to multiple foci of disease in 
insular sclerosis. 

(4) Neurasthenia cerebri, mental fatigue, loss of memory, 
insomnia, loss of will-power, indecision of character, occur¬ 
ring in a young person with a history or signs of congenital 
syphilis might well cause one to consider the possibility of 
the development of paralysis. 

(5) Mental symptoms in the form of melancholia or mania, 



with delusions of persecution, suicidal tendencies, or mental 
excitement with delusions of grandeur and wealth would be 
still more suggestive, and, as some of the cases show, a 
guarded opinion should be given. Absence of pupil phen¬ 
omena and affection of written as well as verbal speech 
should make one withhold a definite expression of opinion as 
to its being juvenile general paralysis, for the progressive 
dementia and the above-mentioned symptoms will certainly 
manifest themselves within a comparatively short period and 
allow of a certain diagnosis. 

(6) Hysteria occurring in a congential syphilitic patient 
might be confounded with the earlier stages of juvenile 
general paralysis, but the presence of hemianaesthesia, con¬ 
centric limitation of the field of colour vision, with the 
absence of the characteristic mental, pupil and speech phen¬ 
omena would settle the point. 

A diagnosis presents fewer difficulties if it be remembered 
that the disease is, pathologically speaking, a generalised 
progressive and regressive metamorphosis of the nervous 
system, affecting as a rule the latest and highest developed 
systems of neurons first. In some of the cases which pro¬ 
gress slowly but surely without complications in the way of 
epileptiform seizures, this was strikingly shown, e.g. (case 
M. G., p. 318 ; case E. N., p. 267), and the symptoms there¬ 
fore can only bear a superficial resemblance to coarse cerebral 
lesions, and only a temporary resemblance to functional 
disturbances of the nervous system. 

Brief notes of a case of well-marked congenital syphilis, 
imbecility and epilepsy, illustrating the effects of syphilis in 
producing arrest of mental development:— 

G. R., formerly inmate of Darenth asylum, sent to Colney Hatch, a 
dangerous epileptic, scarcely able to speak, and only able to use a few 
simple words. He has a low forehead, prominent development of lower 
part of his face, saddle-shaped nose, syphilitic teeth, very marked linear 
cicatrices all round the mouth, stunted growth, large developement of 
genital organs, and has remained in much the same condition for the 
past five years. The fits are epileptic in character, the pupils are equal 
and react to light and accommodation; there is no coarse paralysis, and 
probably this is a case of syphilitic imbecility and epilepsy due to a 
generalised, rather than a coarse, morbid process in the brain, but not of a 
progressive character. (Vide photographic plate iii., fig. 8.) 



Case 1. 

E. N., aged 19, admitted into Caterham Asylum, January, 1897. 

History from the mother .—From the time he was 14 years old the 
boy had been employed at Doulton’s factory up till 17, so that he must 
have been fairly intelligent, seeing that he earned eight shillings a week. 
The mother appears a strong, hard-working woman, and says that she 
has never ailed. The father drinks occasionally heavily, and has knocked 
her about, but he has kept his present place twenty-eight years. She 
gave me the following family history:—Daughter, alive, aged 27; son, 
alive, aged 24; then four miscarriages in succession; an infant which 
lived three months; an infant which lived six months; patient; a 
daughter who is now 12 years of age; then a miscarriage ; lastly, a frail 
little girl, aged 8 years. No insanity, paralysis, or fits on either side in 
the family. She cannot account for her son’s illness, which commenced 
two years ago, when he had to give up his work. He has never had any 
fits to her knowledge.—F. W. M. 

Condition of patient when I saw him .—March, 1898. He is very 
demented, passes urine and faeces beneath him. He is unable to walk or 
stand, and sits in a chair with his hands in his pockets or his arms folded, 
his chin resting upon his breast. The hands are very blue and cold, and 
the face dusky-red and greasy-looking. The pulse is small and com¬ 
pressible. There is very marked tremor in the face muscles, and the 
tongue, w'hen he tries to protrude it, is thrust forward by incoordinate 
jerks ; but he cannot keep it out, and he puts up his finger and thumb to 
try to pull it forward. The pupils are dilated, unequal, and do not react 
to light; but they react, though imperfectly and unequally, on con¬ 
vergence—the pupil the most dilated, the least mobile. He has no 
knowledge of time or place. He has never had any grandiose delusions, 
nor has he exhibited any signs of mental depression. The speech is most 
characteristic, very tremulous and syllabic, and there is so much difficulty 
of utterance that the patient is almost unintelligible; moreover, the 
attempts to speak occasion so much laboured effort that he cannot get 
more than a few words out. He has had no seizures. There are no scars 
on the body, the teeth appear normal, the bridge of the nose is not 
flattened, and there is no linear cicatrisation round the angles of the 
mouth or anus. There are no signs of infantilism. The genital organs 
are fairly developed, and there is hair on the pubes. There is no hair on 
the face. 

August 8.—Patient is very much feebler, he hardly talks at all; his 
appetite, however, is good : he is very incoherent and demented, and will 
not protrude the tongue. He is wet, dirty, and destructive. He has 
emaciated considerably since I saw him. He can neither stand nor walk 
now, and is more helpless and demented than ever. He seemed to 
recognise his mother when she came to see him. The hands are very 
blue and cold, and the pulse hardly to be felt. The pupils are dilated, 



almost equal, and do not react to light. The knee-jerks are markedly 
exaggerated. There is continuous tremor of the lips, and the tongue, 
when protruded, is thrust out in a succession of jerks. He has had no 
seizures, and the most obvious change is the progressive dementia and 
paresis.—F. W. M. 

November 1,1898.—Patient is more feeble and emaciated, but there 
does not appear to be any material change otherwise, or sign of a near 

June 4, 1899.—Eats well, and his condition does not appear much 
changed since I last saw him. He looks more demented. The attendant 
says that he recognises his mother when she visits. He is quite unable 
to speak to her, and he never asks for anything; in fact, he is quite 
speechless. He is quite quiet, does not make any noise or shout, laughs 
in an imbecile manner. He passes his urine and faeces in the bed, but, 
owing to the care of the attendant, he has no bed-sores. He cannot put 
out his tongue, although he will try to do so when told. I do not think 
he is deaf. The feet and hands are very blue and cold. There is marked 
tremor in the limbs, and tremulous inco-ordination on attempts at move¬ 
ment. The pupils, R., 6 m.m.; L., 5 m.m.; inactive to light and 
convergence, irregular. Knee-jerks present.—F. \V. M. 

Case 2. 

B. L., aged 21, admitted into Caterham asylum March 10,1898. 

History from the mother .—She is 61 years of age and her husband 65. 
She had had a large family, of which the patient is the youngest and last. 
There is no history of insanity or nervous disease in the family. She states 
that prior to his birth she had a miscarriage and about that time her 
sight begem to fail her. She went to various eye hospitals, Moorfields 
among others, but she became blind first in one eye then in the other. 
Examination of her eyes showed well-marked disseminated chorio¬ 
retinitis and optic atrophy in both eyes. Her son up to a year ago had 
been able to work. He had never had any fits, but two or three years 
ago he fell out of a van (? a fit), was taken to St. Thomas’s Hospital, 
and since then he has been ailing, but he was able for some time after¬ 
wards to continue his employment of cleaning harness for the Omnibus 

Condition when I saw him .—Patient has an imbecile, childish ex¬ 
pression and speaks in a childish manner and in a very nasal tone. He 
is able to converse and correctly describes his previous occupation and 
where he lived, but his speech is nasal, hesitant, tremulous and syllabic. 
He can stand and walk, but his gait is very unsteady and he walks with a 
wide base, hardly raising his legs. He has a little linear cicatrisation 
about the angles of the mouth and the central incisors are peg-shaped 
and notched and there are linear erosions of the enamel. The tongue is 
protruded by a succession of incoordinate irregular jerks and there is 
marked fibrillary tremor both in it and in the muscles of the face. The 


pupils are unequal, dilated, irregular and do not react to light and but 
sluggishly on convergence. The knee-jerks are markedly exaggerated 
and there is obvious tremor in the extended fingers. His taste and 
smell are good and there is apparently no loss of sensation of touch or 
pain. Examination of the fundi oculi exhibited nothing abnormal. His 
nutrition is fairly good, the hands are somewhat blue but not cold, and 
the pulse is fairly full and strong. Although 20 years of age, there 
is very little hair on the pubes and none on the face. He is under¬ 
sized and pigeon-breasted. The genital organs are infantile. The testes 
are very small, also the penis. His appetite is good, and, according to 
the attendant, he responds to the calls of nature as a rule, thus having 
voluntary control over his sphincters.—F. W. M. 

August 8.—The paresis and dementia are both markedly increased. 
He is now unable to stand or walk, but there is no contracture. Speech 
very incoherent, nasal, syllabic and tremulous. He is continually 
smacking his lips and he has an expression of bien Stre . The pupils are 
unequal, dilated and react neither to light nor accommodation. There is 
continuous tremor in the hands, especially on his attempting to do any¬ 
thing. He cannot write, although he will attempt to do so when asked. 
The knee-jerks are exaggerated, but no wrist-tap contraction is obtain¬ 
able. The arch of the soft palate on each side of the uvula is 
asymmetrical as if there were paresis on one side. The pulse is small, 
thready, compressible and the hands are blue. He has had no seizures, 
but after I had examined him he unconsciously passed a motion. 
—F.W. M. 

November 1.—Patient has gained flesh and his general health and 
bodily condition are if anything better than when last note was made. 
He is more lost, seems to have less control over his bladder and bowels, 
and is quite unable to stand without help. I am informed that during 
the last six weeks he has had what the attendant cedis screaming attacks, 
when he slides down on his back and there is a good of general 
twitching.—F. W. M. 

June 4, 1899.—The patient has emaciated very much since I last 
saw him ; he recognises no one now except his mother. He has had no 
seizures for the last eight w T eeks. He is speechless; occasionally says 
“yes” and “no,” but nothing else. He shouts and cries a good deal. 
Never asks or makes any signs for food or drink ; he has no difficulty in 
swallowing. He tries to put out his tongue, but cannot, instead he 
makes a champing with his lips. Facial expression apathetic and 
immobile. Pupils very irregular, unequal and immobile to light. He 
lays on his left side with the legs drawn up. There is marked con¬ 
tracture and great emaciation of the lower limbs. He cannot move the 
legs and passes his urine and faeces in the bed. There is a bed-sore over 
the sacrum. Upper limbs : the left hand—he can move and hold a 
piece of bread and butter with it; on movement of it one observes a 
marked tremulous inco-ordination. The right hand is much more feeble— 
he seldom moves it; as compared with the left it is more wasted, and 
when at rest one observes continuous and tremulous incoordinate mobile 
spasms in the fingers and thumb.—F. W. M. 



Case 8. 

A. H. B., Darenth Asylum, aged 16, male: admitted April 9, 1897. 
Previous to admission, for three years he had shown signs of mental 
trouble, which was supposed by his parents to be due to an accident 
seven years previously. He was born at full term, labour difficult, not 
instrumental. His health was good until 8 years old. Patient’s father 
a heavy drinker for several years. No epilepsy or insanity in the family 
on either side. There is a history of probable syphilis, seeing that the 
first child died at the age of 6 weeks: then followed two miscarriages, 
then the patient A. B. was bom, and again two miscarriages. The 
medical certificate on admission states:—He is of feeble intellect, and 
deficient in memory and understanding, and has no idea of time or place. 
The notes state that he had tremor of the lips, face, and tongue, and his 
speech was typical of general paralysis. 

I saw him on August 14,1898, and made the following notes:—Patient 
is lying in bed with both knees drawn up, owing to contraction. The 
attendant states that when admitted he could converse and run about, 
but has gradually become weaker and more helpless, and he never speaks 
now, not even to ask for food or drink. He lies there laughing in an im¬ 
becile manner, occasionally shaking his head from side to side. He passes 
everything under him, the urine constantly dribbling away. No hair on 
the pubes, genital organs not small. He recognised his mother when she 
came lately, and he laughed continuously while we were examining him. 
He has been on minced food for the last four months, and for some time 
he put on weight, but recently he has lost flesh. There are no signs of 
congenital syphilis on the body, the genitals are fairly normal, the head 
is well formed, and the face, on admission, did not suggest to the attend¬ 
ant that he was an imbecile. He does not masturbate. The knee-jerks, 
owing to contracture, cannot be tested. The hands and feet are bluish - 
red, owing to defective circulation. The muscles are wasted in arms and 
legs, probably from disuse. Pupils are equal, react sluggishly to light, 
accommodation could not be tested. 

May, 1899.—He is more helpless and demented, he never speaks now r , 
but laughs and smacks his hands on his face and chest; he is restless, but 
not spiteful. He lies in bed on his back, with his knees drawn up. There 
is marked knee-jerk exaggeration and clonus. The pupils are unequal 
and sluggish, but it is very difficult to examine him. I have ascertained 
that his father is dying of general paralysis at Ivybridge Asylum. He 
was previously in 1895 at Clay bury Asylum, when he was said to be 
suffering from mania.—F. W. M. 

Case 4. 

H. I. came to the children’s department of Charing Cross Hospital in 
October, 1892. The mother, who brought the boy, stated that he was 
aged 10. She brought him because there was a lump on his arm. His 
facial appearance was such as to immediately suggest congenital syphilis. 
He had linear cicatrices round the mouth and on the lips, and especially 


at the angles of the month. His teeth are typical Hutchinson’s teeth ; 
the two central incisors in the upper jaw are peg-shaped and notched. 
The speech is nasal and the bridge of the nose rather depressed. There 
is paresis of the left external rectus and pigmentary chorio-retinitis of 
the left eye. Pupils unequal, left larger than right, sluggish reaction 
to light. He is under-sized and badly developed. There is a node on 
the right ulna. His lower limbs are rickety and the shins irregular and 
somewhat nodulated. The mother states that prior to his birth she 
had had several miscarriages and two still-born children before this 
one was bom. She herself has, however, never suffered in any way. 
The next child, a girl, is delicate, but presents no signs of syphilis, except 
internal squint of the left eye. He was put upon mercurial inunction 
and syrup of the iodide of iron. 

On November 28 he came with his mother ; the lump on his arm had 
now disappeared under treatment. She said that five days ago he went 
to school all right, but while there he passed a motion unconsciously. 
He was brought home, cleansed, and returned to school, “ more to get 
him out of the way than for all he learnt, as he was quite an infant in mind.” 
At eleven o’clock he was brought home in a fit and was quite un¬ 
conscious. No clonic spasms, but he remained unconscious from eleven 
to twelve. The teeth were clenched, but he did not bite his tongue. 
The doctor who came gave him an emetic and tickled the back of his 
throat, as he thought that he had been eating some noxious substance. 
When he recovered consciousness there was no paralysis in his limbs. 
According to the mother, he had had a similar but not such a severe fit 
two years previously . Knee-jerks present on both sides; no comparative 
weakness on one side. 

January 18, 1893.—Whilst at school in the morning, the master 
noticed the boy performing rather strangely, for he kept rubbing out 
and re-writing on the slate the same word. He then had a similar fit to 
the one previously described, except that he kept saying “ mother.” He 
remembered nothing about the fit afterwards. When he comes to the 
out-patient department he talks and acts like a weak-minded but good- 
tempered child of 4. He is able to answer simple questions, such as tell 
the day of the month, the time of day, where he lives and the name of 
his master. He can write but indifferently. There is no direct or 
collateral insanity in the family. He continued to come to the out¬ 
patient department till March, 1893, when I lost sight of him till 
Wednesday, September 23, 1896, when my attention was called to an 
interesting case of juvenile general paralysis at Colney Hatch Asylum 
by my friend Dr. Bryan. His appearance is little changed; he did not 
seem to know me and he is very much weaker both mentally and bodily. 
He looks about 10 years old and does not seem to have grown. He does 
not recognise me, talks incoherently, and sings snatches of songs. Asked 
to put out his tongue, he did so. It was very tremulous and jerky and 
there is tremor in the lips; the speech was muttering, hesitant and 
incoherent, although he seemed to partially understand what was said 
to him. The knee-jerks are absent on both sides. The pupils are 
dilated, unequal; the left larger than the right. They do not react 



to light, but react sluggishly on convergence. He does not respond to the 
calls of nature, passing urine and faeces under him (vide fig. 1, plate II.). 


October 11.—Both mentally and physically is getting worse. Wet, 
dirty, incoherent and restless; he is becoming thinner and is in a low 
state of health. 

October 16.—To-day several large bullae, full of serous fluid, developed 
on both feet. The fluid was let out and the wounds dressed with zinc 

October 19.—The above-mentioned bulls have healed up, but others 
have appeared, which have been similarly treated. 

November 4.—Since last note patient has become markedly emaciated. 
He is too weak to stand and has fibrillary tremor of most of his muscles; 
when asked how he is, he can just manage to say “ all right ” in an 
unsteady, muffled voice. Urine and faeces are passed unconsciously. 
Several bed-sores present. 

November 20.—Is becoming still more emaciated. This is most 
marked in the face. He hats not spoken for a week, but lies curled up in 
bed with the corner of his night-shirt tightly held between his teeth. 
Feeding has now become very difficult and he is so weak that the heart 
sounds are barely made out with the stethoscope. 

November 25.—There is little change to record, but he is evidently 

Nov. 27.—Died. 

Autopsy .-^Soon after death. Body very emaciated. Little or no 
hair on the pubes, genital organs those of a boy of twelve. Marks of 
bullae on the toes of each foot, one about the size of a shilling on the 
great toe of the right foot and on the back of the second toe of the left. 
Also one on the plantar surface of the right foot. A dry, dark eschar exists 
over each trochanter, and a similar one over the sacrum. No bruises or 
post-mortem staining. The skull cap is of moderate thickness and non¬ 
adherent to the dura mater, and a considerable quantity of cerebro-spinal 
fluid escaped on removal of the brain. The pia arachnoid is somewhat 
thickened and opalescent over the frontal and central convolutions. The 
posterior part of the brain and cerebellum is not so affected. No patches 
of softening are seen anywhere. The convolutions are rather irregular, 
and those of the frontal appear smaller than natural. The vessels appear 
quite normal, the ventricles are dilated and filled with cerebro-spinal 
fluid, of which 70 c.c. was collected. The ependyma is granular. There 
are a few adhesions over the frontal lobes. Various portions of the brain 
were kept for microscopical purposes. The spinal cord exhibited no 
marked naked-eye change beyond some slight thickening and opacity of 
the pia arachnoid. Thoracic viscera —Except some hypostatic pneu¬ 
monia of the bases, the lungs appeared quite normal. The heart weighed 
only ozs., brownish-red in colour, soft and flabby. Abdomi?ial viscera 
—The kidneys weighed 8 ozs. each, capsule somewhat thickened and 
adherent in places. The organs were tougher than natural. There was 
no naked-eye diminution of the cortex. Liver —Weighed 26 ozs. On 


the right lobe upper surface there was a yellow cicatrix about the size of 
a two-shilling-piece, probably an old gumma. The organ throughout 
was decidedly tougher than normal. There was nothing else noteworthy 
in the intestines or other abdominal viscera. 

P.S .—Since then the mother has brought two younger children to 
me for heinichorea; they present, however, no signs of congenital syphilis, 
and are intelligent children. I have especially warned her against 
pressing them at school. 

Microscopical Examination of the Organs. 

Brain .—After hardening in 96 per cent, alcohol, sections 
were cut and stained by Nisei's method. Ascending frontal 
and ascending parietal convolutions in the middle third show 
microscopic appearances in all respects identical to those 
seen in general paralysis affecting the adult brain. The 
membranes are thickened, the vessels gorged with blood, 
especially the small veins. These vessels are surrounded by 
a dense layer of cells, which are stained by the basic dye. 
Very few of the nerve cells possess any chromatophil 
elements. The nucleolus of the nerve-cells alone is stained 
deeply. The body of the cell and the nucleus is only faintly 
stained. In many of the cells it looks as if only the intra¬ 
cellular network was left. The processes, as a rule, are 
either broken off or can only be traced a short distance. 
The neuroglia cells in the superficial layers of the cortex are 
well seen, and their fine and numerous branches can be 
traced into a delicate network, made more evident by the 
atrophy of the neurons and their processes. The cells, 
especially of the first and second layers, have undergone 
destruction. In the third layer the shadows of the large 
pyramidal cells can be seen. They are but slightly stained, 
and one notices no Nissl-bodies. The swollen pale nucleus is 
evident with its nucleolus deeply stained and connected with 
the periphery of the nucleus by a delicate, faintly-stained, 
intra-nuclear network. The cyto-neuron, or body of the cell, 
has usually lost its normal triangular appearance, the sides of 
the cell are curved, and there is a faint violet colouration, 
due to the staining of delicate fibrils in connection with the 
intra-nuclear network (vide photomicro. 5). It looks as if 
all the hyaloplasm had disappeared, and only the skeleton 

274 . ' AiU'lUVj-s v ; :„ 

uf the fraruewmk of the tu-nron was Theoccipital b<he 
stable*!. by Ni%r method shows a; remark&bW contract to 
the paracentral lnl.»u)e i.rahr phutc.micros <4 ami 4.) The pin 
•oachfjoid is st little thickened, but,all. t.b^‘-,I?»\f. ceils 
IH seen perleoth well, ana the neeashmal larger pyramidal 
fitJ’lW .awe st-ahied quite pormaiTvV showing gray riles fiis- 
fcinefcfy : moreover,' there, is an overgrowth -:>r .gib*.: .eissee 
and -col! .proliferation.... There u ecsifsitleruHe phagoeyi^^ 

Pbotomicrp. of cortex, .showing void 

surrounded Uy; round. 'iix&iirrAtion of pia emciiuoul. The 

purivaseiilyr lyrnpb *[»».« t fe greatly The atrophy of the . U, k 

not appacout. on nmmu t of the 'fey pfiS^ificuUotx, ;; ‘ v ;:• • ;V 


of the cerebral substance 

.;4ii^.hKy;#.O8t4W0!r-' .spinal 

Tn tke britiiP sfcaiiied l4jf.iMtr.chi ,it^hod'^he sniali vessels 

photc-micro. 2). In some places it looks .is if the cells of the 





, .'•’fjhi'Jo't- $$$[& ; : : $ ; £ft * 


• • , 1 i ij! y '■ i&vfi« 

t'WJBHTl-TWO OF iiWstilip.- PAU.vLYblS 27-> 

■are a large number of coarse degenerated fibres in the white 
matter, which would well correspond to the axons of" 
degenerated pyramidal eel's In max* sections of the central 

particles, . toid feheso vessels #c.rii‘ to bendatod in areas of 
adnte irsflauo,de^hiirfttio«V:anct;theappc&raui?es pre¬ 
sented by-them closely correspond with the appearance of 
the vessels similarly stained in prilio-iuyelivis i^.- ng; \, 

iPbotomicro. ‘2.- A srriail vexfv monmg towa/4 1 * fcra cc*rtt;v with a lateral 
bmieb out trftmv*i«$y. ito bp arrount of thi> 

congested blood, Tta pm stained by Aliirphi uipthod, Hud the 'vppfb 
of the external *r«iU- of .Die vein ?* seen oorered 'jyfKfi rpjffe *tyipetl bliiok by 
tbb f*t contained in tiffin up tiro osmio acid. 350 


Stained by M&rehi-Fal method, frontal ttild parietal 
convolutions. also island of ftt*il ; show at* itijdmost total 
absence of taugeutial fibres. • • ■ i by.-iV-vb: 

. Spinal c^rd^'fjtnuhaR enlargement \ stained In; the 

Nfwd'-'Wetbod,. the hbffl obIIs &bbw a fairly normal 

coiiiltioiru l 1 here % tewefvet, a proliferation of glia cells 
around the centra! canal of the- spinal cord. • These cells 

Pbotoniioro. 4. Section 
of occipital lobtv stained by 

Niss! .motnod. Tho definite 
arrangement of fcllff Colia -into 
Slejn ort' k col nmxi* c»vh fe 
” m \, and t-Jiere )5 b rUo <>r 
no inflammation oi iSn 
and pia arachnoid .membranes/ 
Magnification 00 diaui etci> 

rhoiamicro,.. 8. Section 
ot th« attcoiiding frontal, 
-stained by Niast method, 
tense hitlammation 
and glib bell proliferation, 
TUe mft&uinmtory process i» 
-marked as. to destroy 

tfos reguJjfcf biwngwient into 

noiomns of the gang!ion cell*;, 
in /act’, thpy are riot oh^nryable,, 

rtagni^ebtiotj (\o 

Comparo with occipital icb* 

Yvi\ dusi?is ? tiif> ot*]is hi) the pm'vascular iyinplKiin* 
of thv'> an.'l i lioy contain flouring in:ui. y. 


Exfliminritioa of the noiseies,^ affac st;ia£k»ig with Marchv 
fluid,.nof.nttydegeneration. vva^fonntLbuta marked diminu¬ 
tion of striatioii. "tinned with logwood 

and eosm. Epithehmn apjxmra normal. hut. mound the 
vi'-ods tllMO tf.» be Hf) OVergrOWth <>f {foil*: fiblOHS 

tiKhue, Tim capsule is thickened' io places, .'and in these 
situation* th«?re arc advanced degenensiive changes in' the 
glomeruli. Liwr —Sections through - the n<\».y *lmW dense 
fibrous of the capsule, >^0.4 a and 

•pHoto^ie^.&^Sf'ckion of ♦Mitral coiivoiuUoli Ni^l in«Atbt>l, 

] -b-vw • hertta‘3»^ouiinitivo m the [\vn\)!iKHi «.••.•!»;, M>u;mh<:Hti'otr 

‘ of COftr/emtitl v ^pbvlt$. 
Cestk'if -—bhiUmd ot ^fovein lUetimn, •• ii,tS'• - number of 
black particles ip»:e-onmi>! v inmute g;r;tmih:< of igu m tin 
coin,<hMod tubule*. Sectrmn -umrd v.-.ri : moiv..:..,1 ami vosin 

showed no ^/>nuii 1:.'' -'..^, 



Case 5. 

F. A., aged 19, single ; occupation, stationer’s assistant; admitted to 
Colney Hatch June 18, 1896 ; died August 22, 1896. 

The mother was interviewed by me in August, 1898. She gave the 
following history:—He was a bright, intelligent lad, although always 
weakly and delicate. He was a good musician and very sober and steady 
in his habits. His illness had only lasted nine weeks before admission to 
the asylum, and the first thing he complained of was pains in his legs 
and he asked his mother this question : “ Do you, when you have rheu¬ 
matism, have pains in your legs and feel as if they were giving way 
under you ?” A little later he had a delusion that somebody was coming 
to take everything from the house and kill his mother. 

On May 9 he was admitted to University College Hospital under Dr. 
Bose Bradford, who has kindly furnished me with the following notes:— 

“ F A., aged 20, was admitted on May 8, 1896, into University 
College Hospital, suffering with (1) loss of memory (2) headache. 

“ History .—About a month ago patient found that his work was 
getting too much for him and he began to suffer from frontal headache, 
hesitation of speech and shakiness of limbs and loss of memory. 
Formerly played the piano well, but now does not know one note from 
another. Has talked of suicide and also has the idea that some one 
wishes to murder him. 

“ On admission. —Patient is under-sized, thin and pale. Face is 
expressionless. No delusions or eccentricity noticed since admission. 
Speech is slow, hesitating, occasional slurring, but no elision of words 
or syllables. Unable to pronounce some words, as ‘ extraordinary.’ 
Patient reads well. Writing is correct, but shows fine tremor. Both 
fields of vision show no concentric diminution. Palpebral fissure narrow ; 
over-action of both occipito-frontales. Slight rotatory nystagmus. No 
external ophthalmoplegia. Pupils small and equal; do not react to 
light and only slightly to accommodation. No facial palsy, but marked 
twitching and tremor during movements of face. No talipes, but right 
foot is a little inverted and instep is rather arched. Marked lateral 
curvature with convexity to right. No physical signs on chest or 
abdomen. Patient remained in hospital seven days. Only change is that 
delusions have been observ ed, such as accusing other patients of robbing 
him of a bank-book and calling his mother opprobrious names. 

“ Diagnosis .—? Early stage of general paralysis of the insane.” 

Notes on admission to the asylum .—Patient is a thin, pale, very weak 
looking young man, of small stature, weighing only 6 st. 6 lbs. The 
pupils react neither to light nor to accommodation; the tongue is 
tremulous and furred; heart is normal; harsh, respiratory sounds are 
heard all over both lungs; marked lateral curvature of the spine. 
Patient has an ataxic gait, the knee-jerks are absent and Romberg 
symptom is present. Speech is hesitating. He has no delusions so far 
as can be ascertained. He admits long-continued masturbation. 

The mother gave me the following history Her husband drank, but 
always remained in employment. First child would be 89 if alive, it 


fi}^r( of I ^crfOcV^J|ve ,and wdj, aged &8: third alive p then 

two bujffi dead ; mtiMivad to sown mouth-.: g&i? e.jilh is the pathaH. The 
L«Uhi ha* riot keep a steulymiip ; went with other wonion. No infinity 
in Uio family cm. F* \V* M> = * ; . > 

Jime • yyttxMx yMn^ rnan.-' He stood with a wide 

ha&* ftpij a good dad when the. avm wero .^htit. yPuiriia- small, 

irregnW aid reacted neither* to !i#ht not^ncovunediii jOh. He 
wi« the speech wa* hesitant nnd tr&mulacKr npd there, waw 

t-rv»i(!.v iu thy tongue and face unisxdea, The knee*jet’ll were nlrseriL the 
jote-c'leH i>enerall.v waited, hut respond to iarndinm^ wd nppuirnth then* 
wa* hliiufdtig or *?f?n*tttio« all over the body* There War liruwvcu-ntticez 
r»t tiit' tUitjfr.H of the month, the tooth wore very d*rivyed, .and the pey- 
shape and oiifiiilatiun of the central incisom sUggt^fei .tftV: tit 

rbht<m»i'ereo’ H, of lirer, perioapeular. perivascular and porieehOtlkr 

fjhro^ia Sidfndtfoutkm *10... 

td ^WiWife hrul a unil parotic txprd^mu and ’ 

he WM r<uxdy/>vi.\L iti hi*' ? hut • i di*<a> vexed no grandiose delusions 
jahrsfej h||;; S^plateihi ^p&tif£d 

and ¥;or^ht^v:-nhe bfxl-ndfLeu. ; \ _/.•’*./ 

■Aeyu-;‘ If*.—The following hot<> WHH neihe : —J'afknyi hx* wast-d Xv. 

O w ii ;nd _)-.?*>kK nlil>»ud .wrinkled m the t/VCe. Hv u vex. teoMe and * t'U 
i» f dHo taken hl«*-iVn:d .l:tui»v\ Hi- puke h almost 



Post-mortem notes (by H. Chatterton).— Body is much emaciated. 
No bed-sores, bruises, or abrasions. Skull somewhat thin. Brain sub¬ 
stance soft throughout. Ventricles distended with fluid, ependyma 
granular. Membranes thickened in places and adherent over the 1st 
frontal convolutions. Ribs natural. Lungs small and collapsed; no 
adhesions. Heart very small; some atheroma of aorta . Intestines and 
peritoneum natural. Viscera very small and tough. Weight of organs— 
Brain, 38| oz.; heart, 4 oz.; right lung, 4J oz.; left lung, 4f oz. ; liver, 
21J oz.; right kidney, 2$ oz.; left kidney, 2J oz.; spleen 1| oz. 

I was away when the post mortem was made and the brain and spinal 
cord sent to me in M tiller’s fluid w as unfortunately spoiled and had to be 
thrown away. The liver and kidneys were, however, examined, and 
showed an interstitial fibrosis, especially in the liver, where was found a 
diffuse pericapsular, pericellular and perivascular over-grow'th of con¬ 
nective tissue, a condition frequently met with in congenital syphilis 
(vide fig. 6). 

Case 6. 

A. B., aged 23. 

Notes from case-book. —Admitted into Clay bury on January 20, 1896. 
Died December, 7, 1897. Occupation, gilder. Duration of illness, six 
months. Insanity hereditary; tw f o uncles insane, one died in Colney 
Hatch. Father died the year before in Claybury Asylum of general 

January 27,1896.—He is suffering from mania and (?) general paralysis. 
Imagines that a woman has been following him about and that a man 
came into his bedroom to rob him, but when he got up there was nobody 
there. His speech is tremulous and hesitating, his memory appears to be 
good, he has no exaltation, but is somewhat emotional, crying w r hen 
speaking of his father. He denies ever having had sexual intercourse, 
but has practised self-abuse. No history of syphilis. A well-nourished, 
light-complexioned boy, whose father is in Claybury. He has a most 
unsteady tongue, jerking coarsely en masse when protruded. Knee-jerks 
absent. Left eye has internal strabismus, old instertitial keratitis, pupil 
of this eye larger than right. Both sluggish to light and to accom¬ 

July 14.—Mentally he is becoming more demented, interesting as a 
case of general paralysis which is apparently hereditary. He is suffering 
from the same disease as his father at an unusually early age, and 
apparently his life has not been such as to cause general paralysis.—R. J. 

November 20.—The seizure begins with trembling of the hands, 
fingers, and lips. He swdngs his hands about as if to give emphasis to 
his words. He picks at his fingers and shouts, stammers, and clenches 
his hands. Hammers his hands on his knees. His memory for remote 
events is good. He can spell his name ; knows where he used to work ; 
remembers that he lived five months at Reading; know^s that he went 
to school at Cromer Street; know's that he is now in Essex, near 
Woodford Bridge. He is, however, very slow' at grasping questions, and 
rambles from the point into other matters. He stammers, his eyes are 


staring. Pupils unequal, inactive to light. R., 5; L., 4-4$. Paralysis 
of the left external rectus. Old instertitial keratitis. Left eye has a very 
sluggish reaction to light and accommodation. He is troublesome with 
his food and has to be fed. Shortly after this he became worse and 
resisted so much that when an attempt was made to examine him nothing 
could be done. 

December 4.—Patient is now in bed, evidently in extremis . Pulse 
very small and thin. Eyes rather sunken, cheeks fallen in. Respiration, 
36 ; pulse, 140; temperature, 99°. Now pupils dilated, R. larger than 
L.; irregular. Spasms of limbs. Abdominal reflexes on left exaggerated. 
About four days ago he had symptoms of seizure, and was put to bed. 
Ever since has had to have catheter. Has a urethral discharge. If 
pressure is made over the bladder the dent remains. Scar on inside of 
right leg. 

Died December 7, 1896. 

Post-mortem notes (by Dr. White).— Post mortem two hours after 
death. Body poorly nourished. Post-mortem rigidity present. No 
marks. Skull —Normal. Dura mater —Normal. Excess of fluid in 
the sub-dural space and in the sub-arachnoid space. Pia arachnoid — 
Thickened, opaque, scattered adhesions over central and frontal lobes. 
Vessels at the base normal. Brain —Weighed 36} oz. Convolutions 
normal, cortex firm. Vascularity not increased. Ventricles dilated, 
fourth ventricle only granular. Cerebellum —Weighed 5 oz. Left 
pleura —Slight old pleuritis at apex. Lungs —(Edematous. Hypostatis. 
Heart —9 oz. muscular tissue, pale, friable. Atheroma of aorta at base. 
Liver —Weighed 87 oz., fatty, friable, soft. No stones in gall bladder. 
Spleen —4} oz., firm, dark, congested. Kidneys —4£ oz. each, capsule 
strips, cortex somewhat thin. Intestine —Nothing abnormal beyond a 
few patches where the mucosa was congested. No ulceration. 

Cause of death —Exhaustion of general paralysis of the insane. 

Microscopical Examination of the Rolandic Cortex by Nissl s 


(1) Thickening of pia arachnoid with cell infiltration, congestion of 
vessels, dilatation of perivascular lymphatics. Not only the leucocytes, 
which are in abundance in the sheaths of the vessels, are stained blue by 
the basic dye, but also the corpuscles contained in them. None of the 
cells of the cortex show a pyknomorphic condition. They are stained 
faintly blue, and in those sections which have been stained by methylene 
blue and saffranine, the cells are stained a faint dull purple, the processes 
are absent, and the body of the cell, when stained, is seen under a high 
power to be dotted over with a fine dust. The nucleolus alone is stained 
a bluish tinge, and the nucleus swollen up and only faintly stained. The 
blue colour of the corpuscles contained in the blood-vessels I have only 
once seen before. It is possibly due to imbibition of the cerebro-spinal 

The microscopical examination showed that the case was one of 
general paralysis. 



Case 7. 

A. J. R., aged 21. 

History obtained from brother .—Father went out of his mind and died 
about thirteen years ago in an asylum, aged 82, of paralysis. Before 
marriage his father had an accident with a crane, which struck him 
on the head. Patient entered the Navy in 1891 on the training-ship 
“Exmouth.” He was afterwards in the “Impregnable,” in which 
ship he was drafted out to Malta, where he remained for three years. 
During that period he was in the hospital for six months, suffer¬ 
ing from pains in the head. Brother never heard that he had had 
any fits. After serving his three years in the service he was drafted home 
and was for two years on H.M.S. “ Harwich.” He was always a total 
abstainer. He was then drafted to Chatham on the “ Pembroke,” then 
he went to Sheemess and was on the “ Illustrious.” In April, 1898, he 
again went to Malta, and the brother had two letters from him, then 
from August to September he ceased to write; presumably he was ill. 
Then brother had word that he was invalided home. This shows that 
his illness commenced in August or September. In the beginning of 
October he was taken to the Royal Naval Hospital at Southsea, and 
after being there a few days the authorities wrote to the mother to ask if 
she could do with him at home. He was sent home with an attendant. 
As far as the brother can gather, he was quite rational next day. The 
following day he had fifty to sixty fits and had to be held down. 
Brother did not see him, but evidently from his description he had lost 
his reason. Then he was removed to the Poplar Infirmary and after¬ 
wards to Bromley Asylum, Bow. He was there, brother thinks, three 
or four weeks and the brother visited him twice. At the first visit he 
barely seemed to recognise his brother. He had no fits while there. 
The second time he visited him his speech was affected, but he recog¬ 
nised his brother. A younger brother has been in Caterham asylum 
since 1895. The brother, who states that he has always had good health, 
has a broad, flattened bridge of the nose, the teeth are fair and there is 
no linear cicatrisation around the angles of the mouth, but his aspect 
strongly suggests congenital syphilis.—F. W. M. 

I interviewed the mother at her home, but she was quite demented 
and unable to answer any questions. She looked very ill and cachectic. 
The woman in the house said that her son’s death had completely 
deranged her mind. A history of miscarriages or still-born children 
could not be obtained ; the woman in the house said she thought she had 
had several miscarriages and premature births. She had only recently 
become affected mentally. 

June 4, 1899.—I saw the younger brother of patient, an inmate of 
Caterham asylum, and the observations I made upon this patient fully 
confirm the syphilitic history. 

H. R. R., admitted to Caterham asylum August 11, 1895, aged 16. 
He was stated to be feeble with arrested physical development and con¬ 
genitally weak-minded. He is clean and able to attend to his personal 
wants, but quite incapable of taking care of himself or of earning his 


He is an under-sized but not physically malformed man; he has an 
imbecile expression and a yellow, earthy complexion, He answers ques¬ 
tions fairly well. He has a fair knowledge of time and place and can 
give a rational account of himself and his doings. He tells me that 
he went to school and passed the 2nd standard. He wrote his name in 
my book. There is no tremor in his speech or writing and he has had 
no fits. Hearing and sight good. Muscular development very fair. 
Pupils equal, regular and react to light and accommodation. 

Signs of congenital syphilis. —Characteristic saddle-shaped nose, 
nasal speech; breathes through his mouth. He had bad eyes when 10 
years old; he has now opacities of the upper edges of both corneas (very 
like an arcus senilis). There is slight linear scarring at the angles of the 
mouth. Teeth: Upper jaw —Two central incisors linear erosion of the 
enamel, lateral incisors rather peg-top shaped. All the lower incisors 
have marked linear erosion of the enamel in the upper third of the cusps; 
they are small, ill-developed and taper down towards the sockets so that 
there are considerable spaces left between them. The skull is asym¬ 
metrical, small; frontal development imperfect. There is a well- 
marked ridge along the line of the interfrontal and interparietal junction 
and a less marked ridge at right angles to the same along the inter- 
fronto-parietal suture. His ears are set low and with planes set, so that 
the upper part of the ear projects. 

There can be no doubt, therefore, of congenital syphilis existing in the 
members of this family, and the facts observed in the above case are of 
great importance in the history of the patient whose notes are subjoined. 
—F. W. M. 

A.R., male, aged 21, single; admitted into Clay bury Asylum on Decem¬ 
ber 8, 1898, under the following medical certificate:—Patient seemed 
mentally lost; he stared about with a Lightened expression; he speaks 
with great difficulty and unintelligibly. Asked how old he was, he said, 
“ M right." Duration of attack about six weeks; father died in Banstead 
Asylum. Condition on admission: height, 5 ft. 2 in.; weight, 9 st. 
4 lbs ; four good vaccination marks on left arm; old paper scar on right 
shin; palate vaulted, teeth fairly good, appetite variable, bowels regular; 
urine 1010, no albumen, phosphates. Heart, pulse, lungs, normal. 
Pupils are unequal, and react sluggishly to light. Gait normal; reflexes 
present but diminished. He is quite unable to give any account of 
himself. When asked questions he grins and makes some absolutely 
unintelligible reply. Appears quite lost, and does not take any intelligent 
interest in things going on around him. He speaks slowly and very 
indistinctly, and drawls his words. Face expressionless, pupils unequal, 
right the larger; both pupils react sluggishly to light. He is grossly 
demented, but at present he is clean in his habits and well nourished. 

December 6.—He is suffering from primary dementia. He is dull, 
stupid, listless and vacant. He is unable to give his name or in any way 
to account for himself. He smiles and grins in a lost, stolid, imbecile 
way. He has no idea of time or place. He masturbates, and the 
attendant tells me that the patient himself made him understand that he 
had had fits, but I cannot make him understand anything. On this date 



I saw him in a typical epileptic fit, with conjugate deviation to the left. 
He is in fairly good nutrition. Gives to me the appearance of being 
blind from his stare. His pupils are unequal, and the right is larger; 
both react very feebly to light and convergence.—R. J. 

December 7.—Last evening, between six and nine p.m., he had eleven 
convulsive attacks; the first was epileptiform in character, affected both 
sides, and he had deviation of the head and eyes to the left, there was 
no aura, no cry, but a short tonic stage. After this first fit he seemed to 
lose all power in his right side, and the subsequent convulsions started 
from the left ankle and implicated the left side. They merged one into 
another, were simply convulsive attacks without any tonic spasm. He 
was quite unconscious, pupils widely dilated and would not react to light; 
stertorous breathing, and a considerable accumulation of mucus in his 
air passages. He was somewhat cyanosed and perspired profusely. 
Heart sounds, first very short and flapping; second indistinct, rate 180. 
His temperature gradually rose to 108*2° in the rectum. He was sponged 
with iced water and his temperature came down to 108°. A simple enema 
was given, and subsequently 40 gms. of chloral and a hypodermic injection 
of two drachms of brandy. His heart sounds improved, pulse became 
fuller and less rapid. He regained conjunctival reflexes and pupils 
became small and contracted, but he never regained consciousness, and 
died at 4.55 p.m. He had no convulsions since 9 p.m. the previous 
evening.—F. Piper. 

Post-mortem notes .— Post-mortem about seventeen hours after death, 
the body has been in the cold chamber since death, but was not suspended. 
Body well nourished and muscular. Post-mortem rigidity passing off; 
post-mortem lividity over dependent parts. No external marks or bruises, 
old tissue paper scar over inside of right knee, and another over right 
shin, with thickening of periosteum, the latter probably due to injury. 
Two small scars on the outside of right foot. No scar on penis, no 
indurated glands. Pupils dilated equally, mm. No hair on chin, but 
commencing on upper lip. Hair on pubes scanty; reproductive organs 
small. No thickening of dura mater. Subdural space slight amount of 
fluid. Pia arachnoid thickening over whole fronto-parietal regions, 
especially so over base of first and second left frontal convolutions, and 
along Sylvian fissures. Veins appear very congested even through the 
dura. Superior longitudinal sinus filled with dark clot. All sinuses full. 
Basal arteries not thickened. General venous congestion. Weight of right 
hemisphere 520 grins., left hemisphere 500 grins. Atrophy of posterior 
parts of first and second frontal gyri, more so on left than right. Very 
granular ventricles, large quantity of fluid, no great distention. Left 
lateral ventricle shows greatest dilatation. Fourth ventricle very granular. 
Cerebellum, pons and medulla weigh together 160 grins. Cord appeared 
slightly soft throughout, and there is slight oedema about the lumbar en¬ 
largement. Thyroids enormously swollen. Tracked —mucous membrane 
congested and oedematous. liight pleura adherent at apex and whole 
of left pleura adherent (old). Bronchi —great congestion of mucous 
membrane. Lungs —right 750 grms., left 600 grms., both congested, but 
crepitant all over. Pericardium—no fluid or adhesions. All heart valves 


Photograph 1. H^ii mvturaj size of the livev. A. J. K. Case T. 

lihrous tissuo. Tho right lobe* h* uUo nodular in }daces, and the cup*Yik? 
h lii'i'i* itnd thHTf thickened so tliat portion** of the organ ;u>* piitthiily 
separated. The tdijes of tiv: right. John are■ rounded and upon the upper 

'■'tiffjgm K\y? 

l.s c#v£ tT^ 

pk®8*! : 

i\V(. • ' 

V : ,V < r*KtjSf 


- Hfjn ** ,; E25Ca • r*i< 

S 1 . * 4 •'* 



surface there are three small tallow-like spots. Section of the organ 
appears like a nutmeg. Gall bladder —Little bile, dark, no gall stones. 
Spleen —220 grms. Capsule thickened and adherent, small tallow-like 
spots on capsule. Substance congested. Malpighian bodies distinct. 
Kidney —Left 180 grms. Superficial patchy thickening of capsule. 
Organs congested and greasy-looking. Capsule strips readily, organ not 
lobulated. The right weighs 150 grms. and presents the same appearances 
as the left. Bladder —Full of dark urine. Weight of bodies of testicles 
together 20 grms. Alimentary canal —Normal.—F. W. Mott. 

Microscopical Examination. 

Tissue stained by Marclii method. 

Heart —Universal fatty degeneration. Thumb muscles — 
Very early fatty degeneration. About one in ten fibres. 
Pectoral muscles —Very early fatty degeneration. About one 
in three fibres. Diaphragm —About one in three, but fatty 
degeneration much more advanced. Kidney —Very marked 
congestion. Intense early fatty degeneration of the renal 
epithelium of all the tubules. It does not, however, seem to 
have attacked the glomeruli at all. Liver —Intense fatty 
degeneration of every part of the lobule. Unlike most other 
cases, the cells in the central portion of the lobule are as 
much affected as those at the periphery. Perivascular and 
pericellular fibrosis. Enormously congested capillaries. 
Testicle —The epithelium of the seminiferous tubules of the 
testicle shows the same fatty degeneration as the epithelium 
of the renal tubules. 

Tissues stained with logwood and eosin. Liver —The 
left lobe and also portions of the right lobe were ex¬ 
amined. The pieces of tissue taken for examination were 
several of the botryoidal lumps with the dense fibrous 
tissue connecting them, also a portion of the organ where 
the capsule was thickened. The liver cells do not stain 
well. The vessels are extremely congested, and there are 
numerous extravasations of blood. The dense fibrous tissue 
strands which separate portions of the organ entirely from 
one another are infiltrated with round cells, and there are 
numbers of new bile ducts. The vessels in the fibrous 
tissue are extremely congested. The inflammatory process 
which has resulted in the formation of scar tissue with 
round-celled infiltration extends along the vessels as far as 


the terminal divisions of the portal canal, but the extent of 
the process varies very considerably in different situations ; it 
does not appear to extend into the interlobular vessels, and 
therefore there is no pericellular fibrosis. Dr. Barrett, who 
has given much time to the study of the process of experi¬ 
mental atrophy and fibrosis, does not consider that this was 
produced by a primary obstruction of the bile duct. He 
would regard it as a very old process. Testicle —Appears 
fairly normal. There are numbers of spermatoza seen in 
the spermatic tubules. Kidneys —Marked congestion but 
no haemorrhages seen. The capsule is somewhat thickened, 
but there is no extension of the process into the substance 
of the organ. The epithelium in the tubules appears fairly 
normal, for I cannot find a single tubule which is not lined 
with cells having a well stained nucleus, but the body of the 
cells may possibly be changed. The tubules appear dilated, 
and filled with coagulated granular material. Heart — 
Appears normal except that the striation of the fibres appears 
completely lost. Cerebrum —Top of ascending frontal and 
parietal convolutions stained with Gudden’s carmine shows 
thickening of pia arachnoid with cell infiltration, congestion 
of vessels and haemorrhages. The vessels entering the 
cortex are congested, their pericellular lymphatics filled with 
cells, and some are here and there surrounded with spider 
cells which send their processes on to the walls. There is 
atrophy of the molecular layer, with great increase of spider 
cells. The regular serial arrangement of layers of the ganglion 
cells is lost, and the cells themselves are in all stages of 
atrophy and degeneration. Examination of Broca’s con¬ 
volution on the two sides by Marchi-Pal method revealed 
complete absence of the tangential system of fibres. Exam¬ 
ination of a slice of brain, consisting of the base of first 
frontal, the ascending frontal, and the ascending parietal by 
the same method, showed complete absence of tangential 
fibres in the two former, and almost complete absence in the 
latter, but there were a few fibres left in the ascending 
parietal. Spinal cord —Lumbar and cervical enlargements. 
Tenth thoracic stained by Nissl method. Vessels —Venous 
engorgment of the vessels in the roots. Infiltration of mem- 



branes with leucocytes. The central canal of the spinal 
cord is filled up owing to proliferation of glia cells. Lining 
epithelium not recognisable. The cells have the appearance 
of being in little colonies. The cells of the anterior horn 
show a fairly normal appearance, except perhaps the dendrons 
are attenuated, and as a rule show no secondary or tertiary 
branches, but the nucleus is not swollen nor is the chromatic 
substance as a rule altered in appearance nor diminished in 
quantity, although some of the cells show at the periphery 
slight chromolytic changes. The spaces in which the cells 
lie are increased in size; this, however, may he due to 
shrinkage, for the cells do not present an abnormal shape. 
It will be observed that, although the temperature went up 
to 108 ’ just before death, yet the anterior horn cells of the 
spinal cord showed the Nissl granules fairly well. If, there¬ 
fore, hyperpyrexia produces dissolution of the granules it 
takes a certain time to do so.—F. W. M. 

Case 8. 

W. M., aged 20, admitted into Colney Hatch in June, 1898; occupa¬ 
tion, clerk; single. First attack came on when he was 18, and he has 
been affected on and off for two years. No epilepsy; no suicide. Mother 
and paternal grandmother said to be affected with insanity. 

Facts indicating insanity observed- by medical men .—He is unable to 
speak, makes inarticulate noises and foolish gestures, takes no notice of 
questions, is very dirty, and has to be looked after in every way. 

August 10, 1898.—The patient is lying in bed with his knees drawn 
up; he does not speak. When asked to put out his tongue he does so. 
but with difficulty. He spits at you if you go near him, and he is con¬ 
tinually smacking his hands and chest. He swallow's his food when fed. 
He does not obey the calls of nature, but passes his urine and faeces 
beneath him. He is very emaciated. Hair is commencing to grow on 
the chin and upper lip, and the hair on the pubes is fairly abundant. 
The testicles and penis are not large, but they are not disproportionately 
to the body small. There is excessive knee-jerk obtainable on both 
sides, also WTist - tap contraction. The pupils are slightly irregular, 
equal, and do not react to light, or only very sluggishly. It is impossible 
to test accommodation, for the light reflex can only be tested by forcibly 
opening the eyes. There are no signs of syphilis on the body. The 
teeth are normal and w r ell formed. He cannot stand. The hands and 
feet are blue and cold. The superficial reflexes—abdominal, cremasteric, 
and plantar—are easily obtained. It is impossible to test sensation, but 
when pinched he shows signs of feeling. 


I wrote to the father, but could not obtain any family history other 
than that contained in the case-book, which was of no use to me. 

This turned out to be a case of general paralysis, as I had anticipated, 
but I did not see the autopsy. Pia arachnoid thickening over frontal and 
central convolution was found, with adhesions. Excess of cerebro-spinal 
fluid, granular and dilated ventricles. 

Case 9. 

A. S., admitted September 4, 1895, aged 18; male. No insanity in 
family. Father died of pleurisy. A brother and sister alive and well; 
several died at birth . 

Patient had a fall in infancy after he had learned to walk. The 
doctor who attended him thought it would be fatal; he, however, reco¬ 
vered, but he had to be re-taught to walk, and many other things. He 
had not grown at all since the age of 12 or 18. For three years prior to 
admission he had been often in the habit of wetting his bed. He was 
mentally quite well till fourteen months before admission. He had a 
fright then. Nine months before admission he had his first fit, and he 
was more or less unconscious for several days afterwards. He had a 
succession of these seizures fourteen days before admission, and was 
again stuporose. Afterwards he seemed foolish and very strange ; atten¬ 
tion difficult to find; incoherent in remarks; would shout; would repeat 
phrases over and over again ; dance and whistle. 

Admitted in a very fair state of bodily condition. Very small for his 
age, 55 inches high, and girth at level of nipples 26£ inches. Weight, 
5 st. 7 lbs. Palate normally shaped. He looked much younger than 18. 
Genitals were the size and development of a boy of 11 or 12, and with 
the merest trace of pubic hair ; no sprouting of hair on face at all. Gait 
unimpaired. Knee-jerks exaggerated and all superficial reflexes very 
brisk; pupils reacted to light and to accommodation. Tongue and lips 
tremulous. He was excited, whistling and shouting during examination 
in a vacant, stupid manner. Tossed his arms about. Questions had to 
be repeated several times. Urine free from sugar and albumen. He 
quieted down, but often relapsed; but all the time till his death, some 
sixteen months aftei admission, he varied, and was generally more or 
less noisy and restless, requiring side room at night often, sometimes 
extremely excited, raving, shouting, kicking, whistling—all in a very 
vacant, stupid manner. Attention never properly roused, nor did he ever 
connectedly converse. Three weeks after admission he had a succession 
of seizures, and again a week later; they affected principally the left 
side; head turned to the left during a fit. From time to time he had 
these severe seizures always much more like general paralytic than 
epileptic. At times the left side would be paralysed, but only tem¬ 
porarily. Began to get thinner six months before death, and then 
slowly but steadily went downhill, and showed very great wasting. 
Developed wet and dirty habits. A fortnight before death a sore 
developed on each trochanter. Death from pneumonia of left lung. 




Post-mortem —Sixteen hours after death. Temperature 40°. Nothing 
in general viscera save pneumonia; consolidation of left lung and two or 
three small ulcers in stomach, close to pyloric opening. Brain weighed 
1210 grins., as it was removed from skull with pia on it. Pia arachnoid 
thickened and opaque, especially in frontal parietal region, and over this 
region it presented most typical general paralysis adhesion. Much 
excess of cerebro-spinal fluid and much wasting of convolutions, espe¬ 
cially the superior frontal gyri and those of super-parietal lobule. Lateral 
and fourth ventricles had numerous and well-marked granulations of the 

Case 10. 

J. D., aged 20, male, admitted August 27, 1892, with a history from 
the Union of having l been restless at night; would not stay in bed; 
wanted to go and look after horses which did not exist. Heard voices 
at night and shouted to imaginary people. 

Certified as being rambling and incoherent in speech. Spoke of 
various engagements at music-halls and that he had been ordered to look 
after horses. Boastful. Spoke of guns and cannon-firing. Offered to 
fight. No personal, previous, or family history obtainable, but he had 
typical evidence of congenital syphilis in his teeth and in linear scars 
round corners of mouth and had rather a blob nose. A little scarring of 
cheeks and chin. 

On admission he was stout; weighed 9 st. 5 lb.; short stature. Ex¬ 
pression vacant and somewhat imbecile. Knee-jerks exaggerated, with 
some ankle clonus. Pupils react sluggishly to light, were equal, but the 
right very irregular in outline, apparently from an old adhesion, and the 
cornea had a slight opacity. He spoke in an off-hand, rambling fashion. 
Thought he was an M.P. and that the ward was the House of Commons. 
Thought he had engagements at numerous theatres. Memory a blank 
for time, but he could recall certain past events in his life. In behaviour 
he proved noisy and mischievous; gave much trouble. Always ready 
with a smile and would laugh inanely. Gait became distinctly spastic. 
Never any nystagmus. Speech quite like that of a general paralytic. 
Two and a half months after admission he had a typical seizure and 
it was afterwards found that he had lost the use of his left arm and 
leg, and dragged the latter for some time. Between this and June, 1898, 
he had several seizures and he became generally more and more paretic. 

I saw him in July, 1898. He then had become helpless; could not 
walk; spent his time in a chair or in bed. He was fat and bloated ; 
skin greasy. Expression silly, but intensely happy. Entirely failed to 
realise he was weak. Showed bien etre , but had become too demented 
to express his former expansive delusions. He could state his name 
and age and where he had lived. All reflexes on both sides were much +. 
Tapping one side would often elicit them on the opposite. Tactile 
sensibility normal, but sensation to ppin as tested with a pin was ex¬ 
aggerated. Pupils both irregular in outline ; fairly equal ; reacted 
faintly to light. Tongue and speech tremulous. I then diagnosed him 


as a case of general paralysis. Three months later troph c lesion com¬ 
menced to form. Two months before death he developed a cough, and 
examination showed consolidation at left apex. He then began to lose 
flesh very rapidly, developed more sores, and died on November 8, 1898, 
that is, fourteen months after admission. 

Post-mortem .—Skull cap not thickened, but very dense. Much sub¬ 
dural fluid and everywhere cerebro-spinal fluid was in excess. The pia 
arachnoid showed many cortical adhesions over frontal parietal region. 
Not much convolutional atrophy. The brain weighed 42} oz. 

I am indebted to Dr. Bond for the notes of Cases 9 and 10. 

Case 11. 

F. P. C., 1 aged 17, was admitted into the London Hospital on March 
6, 1899. 

Family history .—Father died, aged 58, from erysipelas, and the 
mother died, aged 48, of consumption. She spat phlegm and wasted, 
which lasted for two years. There is no collateral history on the father’s 
side, and the mother had no brother or sister. There are definite signs 
of syphilis. The first four children died in infancy. Sixth twins : (1) died 
shortly after birth ; (2) informant, who is alive and healthy. Seventh, 
eight, ninth, tenth, and eleventh are living. Twelfth is the patient. 
Father married second wife in November, 1887. There are two children, 
both living. Father died in 1890. Second wife in 1890, in confinement. 

History from brother .—Patient has been ill for ten months. He was 
first noticed to stumble when he walked. He has lost his memory for 
ten months. He went to school between 5 and 6, and left at 18. He 
was in the sixth standard. He got on very well at school. On leaving 
school he was put to work, first at a paper office, then at a wine mer¬ 
chant’s. It was first noticed that sometimes when he was told to do 
anything he did not seem to understand. No history can be obtained of 
fainting fits. 

History from patient .—Says that he has been ill since Christmas. 
Was at a wine merchant’s, “labelling bottles and that.” “First time 
I ever went there I came over queer.” “ About two years ago.” “ Some¬ 
times I fainted and that.” “Left place Christmas Eve.” “Used to 
help my brother and label bottles.” Went to Rushmore Road and 
Greyhurst Road, Dalston, Board School. He liked school and got on 
well. Was taught geograghy and science. Says that his memory has 
been getting bad “ since I left wine merchant’s.” 

Patient is 17 years of age, but looks like 12. He is very small, being 
only 4 ft. 4 in. He has a broad, flat face, and his ears are set low, and 
with planes set so that the upper part of the ear projects. The measure¬ 
ment around the head, passing just above upper part of insertion of ears, 
is 21 ins. There is an extremely marked transverse ridge in skull over 
vertex, just in front of level of insertion of ears. There are three quite 
definite scars at the right angle of the mouth, one scar at left angle. 

1 am indebted to my friend, Dr. Head, for the notes of this case. 



The teeth are not notched, but the two upper incisors are deficient in 
enamel at their cutting edges. The six-year-old molars on both sides 
have a furrow running round the crown, just outside the summit of the 
cusps. This is especially well seen on the right side. He says that he 
used to have fainting attacks, and has fallen. His speech is typically and 
profoundly altered : all R’s are slurred. Has marked difficulty in begin¬ 
ning each group of words, with stumbling over first syllable. Marked 
slurring of the middle of the words; “ Dalston ” becomes “ Dawston.” 
No alteration in resonance or phonation. Patient walks on a rather 
broad base, with his knees a little bent. There is no staggering with 
eyes shut. Much tremour of both hands, but the left particularly 
tremulous; neither grasp good. There is no paralysis, but there is 
weakness of the coordinated movements of both extremities. He can 
approximate the thumb to his fingers one after the other (both tips and 
bases), but does so slowly and with much tremor. He can touch the tip 
of his nose with his forefinger, both with eyes shut and open. When told 
to do this he begins with the index finger, and then goes on to the other 
fingers in succession. Both hands and both feet are blue, and the circu¬ 
lation is very feeble. This is especially the case with the hands, which 
show marked vaso-motor disturbance. There is no tremor apart from 
that of the terminal portions of the limbs in attempts at coordinated 
movements. Both his knee-jerks are exaggerated; no ankle clonus. 
The left wrist tap is a little exaggerated, and the jaw-jerk decidedly so. 
His pupils are of large size, and react sluggishly to light; doubtfully to 
accommodation. The right pupil is slightly larger than left; this 
inequality is much more marked at times. The left pupil tends to be 
•oval, while the right is circular. There is no ptosis, nystagmus, or ocular 
paralysis. There is extremely marked tremor of the face, especially w T hen 
he opens his mouth. This is very noticeable on talking, especially in the 
muscles around the lips. There is no marked flattening or loss of expres¬ 
sion, and no inequality in the two halves of face. There is extreme 
general tremor of tongue. Palate moves well. Sometimes he has to go 
to pass water very quickly, but has not wetted himself or passed motions 
into trousers. 

Vision .—L. V., R. V., . With glasses: L. /g, badly; R., §, 

nearly perfect. 

Ophthalmoscope. —In the left fundus there is a w r hite patch of chloroidal 
atrophy, surrounded by black pigment: none elsewhere. There is no 
optic atrophy in either eye. Hearing very difficult to test, but apparently 
good. Smell and taste good. 

Mental state. —Quiet and orderly, grateful, easily managed, and 
patient. Sits or wanders somewhat aimlessly about. Quite happy and 
cheerful. Talks to the other patients. Takes food well and cleanly, but 
is tremulous. Can dress himself slowly, but has some difficulty with his 
buttons. Denies that he has ever wetted his trousers or passed water 
into bed lately. Certainly does not do so habitually. Speech profoundly 
altered. Marked slurring of words with elision :—A / spekbl ' w - oomaii 
was chargd / h - / ousbreakn / . There is a very marked increase in 
the number of the breath pauses. During reading there are irregular 


sounds made by tongue and lips heard, which have no relation to the 
word sounds which he is pronouncing. These irregular sounds may 
occur at the beginning of any syllable. The most marked is formed 
apparently by “clicking of the tongue” against the front part of the 
palate, followed by a licking of the lips (like as with a speaker whose lips 
are dry). He fails to carry out movements involving a triple choice, and 
even hesitates over movements involving a double choice. Gives left 
hand for right; withdraws it, and gives right. Sleeps well. Has no 
hallucinations. His memory is bad. Says he came to see me three 
weeks ago (one week), then afterwards got to last Thursday (correct), and 
stuck there. He cannot remember more than the names of what he was 
taught at school—“ Physiology, geography, arithmetic.” Remembers no 
fact in either of the two first, and cannot perform any operation in arith¬ 
metic ; 10 + 12 = 18. 2 x 4 he gives quickly as 8, but is at once puzzled 
by 4x2. This came off several times. His knowledge of time and 
place is good. Knows date of week and month, but tends to get his year 
wrong. “ Says it is 1900 ” (Jubilee was 1894). Knows he is in London 
Hospital. Knows how he came and how he is going to get back. His 
coherence is good so long as he is allowed to state his own story. Easily 
gets confused. Gives vivid and accurate descriptions of how he went to 
Mudie’s for his master, and got caught in the Lord Mayor’s show. Asked 
the date, says 1897 (at this time he was not working for that master). 
Has no delusions; no grandeur. When he has once made a statement 
he sticks to it. Not unfrequently he says he “does not know.” He 
complained of “ queerness that comes over him sometimes,” but says he 
is much better now. 


Case 1. 

Summary. Hereditary insane indirect. Syphilis direct. Congenital 
deficiency. Congenital syphilis. Convulsive seizures in early 
stages. Progressive dementia and paralysis . Speech markedly 
affected and eventually lost. Deep reflexes exaggerated. Pupils 
affected . Never menstruated. Duration seven years . Commenced 
at 12. Death , exhaustion . Typical naked-eye and microscopical 
characters of the disease. Left hemisphere weighed 49 grams less 
than right. 

E. E. G., aged 19, single; no occupation. Admitted into Hanwell 
Asylum on November 17, 1898. 

History. —Patient’s father served seven years in the army, but was 
never abroad. His habits were very dissipated before marriage. He 
took up the occupation of carpenter and married. After marriage his 
habits became worse, was frequently drunk, and he died suddenly at the 
age of 41. The cause of his death, as ascertained by post-mortem 
ex aminat ion, was heart disease. It is said that for six weeks before his 
decease he was never sober. He most probably infected his wife with 
syphilis. His brother was an inmate of Caterham Asylum for Imbeciles. 



No insane hereditary could be obtained on the mother's side. Her habits 
seem to have been good and her mode of life regular, but she had more 
than her share of trouble, owing to her husband’s loose manner of living. 
The history of her pregnancies was as follows:—She was 24 when 
married and has been pregnant ten times. The first was born dead at 
six months. Before her second there was an interval of six years. 
Then, second, was a premature birth of twins. The third was bom dead 
at the fifth or sixth month. The fourth was the patient. The fifth to 
tenth were bom alive and are now living and healthy. 

Personal history .—Patient was a full-timed child and her birth was 
uncomplicated and natural. She w f as delicate and had snuffles, but no 
rash on the buttocks. Her eyes were always healthy, but the milk 
teeth were bad. Mentally she was always deficient and could never be 
taught to tell the time or to read or write. She was sent to school when 
6 years old, but was removed at the request of the schoolmaster, who 
considered her education hopeless. At 12 years she had her first fit 
when playing in the street. She suddenly w'ent unconscious and lay for 
one and a half hours with her face pale and lips blue and her eyes open. 
There were no clonic spasms, merely fumbling movements to the 
pockets. She neither frothed at the mouth nor passed her urine. The 
sudden decease of her father occurred w'hen she was 16 and affected her 
profoundly. From this time she gradually got worse, becoming day by 
day more childish. The second fit occurred when she was 17 and w f as of 
a similar character to the first. It was now noticed that she dragged 
her legs wiien walking and began to lose flesh. This increased until 
nine months ago, when she was put to bed. Speech was noticed to be 
profoundly affected two months after. About this time she had a 
pemphigoid rash, widely distributed, which itched and left scabs. She 
became very spiteful, biting those who came in contact with her. Three 
months ago her friends noticed that she had visual hallucinations. She 
became so bad that she had to be removed to the workhouse infirmary, 
where she was certified and sent here. Menstruation w r as never 

Condition on admission. —Patient’s development was nearer that of a 
child of 12 than that of a young woman of 19. She w as short and thin ; 
masculature, flabby. Her hands and feet were cyanosed and cold. 
Her temperature was subnormal. There w'ere no injuries or bruises. A 
small parchment scar w*as present on the left temple and several on the 
legs. A small bed-sore was present over the left sacral region, and the 
skin, especially of the legs, w p as coarse and scaly. There was no 
varicosity and no fractures, recent or old. Her hair was scanty, thin and 
fell out and the scalp was dry. Frontal eminences were prominent, 
especially the right. A ridge was present in the position of the inter- 
frontal suture extending into the sagittal. Her complexion is good but 
pale. Scar as noted. Face not deformed. Hair brown and partial 
ptosis of the left eye-lid. Her lips were cracked and sore, but there were 
no scars about the mouth. Patient refused to protrude her tongue. 
There were marked tremors on movement of the facial muscles, especially 
the naso-labials. The contraction of the two sides of the occipito 


frontalis was unequal, the right contracting more vigorously. The palate 
was high but not deformed; the alveolar edge, however, tended to be 
elevated and to be thrown out in front. Her teeth were decayed and the 
lateral incisors peg-shaped. Gums were tender, ulcerated in places and 
bled easily. There was no marked deformity in her ears. Her fingers 
were long and markedly striated longitudinally. Genua valga was 
present and inversion of the feet, both sides. Also flat foot. The knees 
lay to the right side of the bed. There was some development of pubic 
hairs. Mammae very small and nipples undeveloped. The thyroid 
gland was not enlarged. There was no other deformity present except 
great prominence of the stemo clavicular, articulations and a degree of 
lateral curvature of the spine. The peculiar movements were those of 
picking the bed clothes. There is marked paresis of both legs, knee- 
jerks markedly exaggerated, knee clonus present, a tap on anterior tendons 
on the leg caused a spasmodic contraction. Plantar reflex present. 
Ankle clonus was obtained. A degree of rigidity at the knees. Exag¬ 
gerated deep reflexes of arm. Wrist-tap present and exaggerated. Volun¬ 
tary movement of muscles caused marked tremor. Muscles of arms and 
legs much wasted. Pain sensation is present everywhere. Tactile could 
not be investigated to any profit. Sight —No keratitis, partial ptosis of 
left eyelid. Left pupil dilated and immobile to light. Right somewhat 
contracted, and reacted sluggishly to direct light. Right eye, and probably 
left, reacted to accommodation. The margin of the left pupil was 
irregular and placed eccentrically. Conjunctive normal. Hearing, taste 
and smell could not be investigated. Co-ordination , gait , dc. —Move¬ 
ments were very inco-ordinate. Patient cannot stand without support. 
Tremulous movements of face and hands. Tremor of stemo-mastoids 
marked. The superficial reflexes of the abdomen are exaggerated. 
Speech —Voice is tremulous and interrupted. Could say a few simple 
words like “ don’t,” “mother,” but she mostly expressed herself in sense¬ 
less noises. There were no cardiac murmurs, the respiratory sounds 
were normal, liver dulness not enlarged, constipation present. 

Mental state on admission .—Attention difficult to obtain. Appeared 
to understand simple questions, but was unable to frame a reply. Was 
not cognisant of her present state, and failed to orientate. Was said to 
have visual hallucinations, but no evidence found. Intellectual grade 
low, and education m7, being unable to read or write. Was somewhat 
noisy and restless. Her efforts at speech resulted mainly in incoherent 
unintelligible verbigeration. Was spiteful, and attempted to bite my 

Progress since admission .—Was found to be wet and dirty. No fits 
have occurred since admission. Has been unable to sleep and has required 
hypnotics. Great difficulty was found in feeding her, but in this respect 
she has improved of late. She has lost her spitefulness and is now' quite 
’gentle. She kissed my hand like a child this morning (December 18). 
She was able to get up for half the day for four days after admission, but 
lias been confined to bed since. The bedsore improved for a time but 
lias got worse since. She has become much weaker and the lower 
extremities are now nearly completely paralysed. I have given her a doll 

4 296 


with which she is very pleased and seems to enjoy nursing it. The lower 
limbs have acquired a greater degree of rigidity since admission. She 
cannot produce any word now; she only repeats the same unintelligible 
noise. Has not menstruated since admission. 

Duration .—Probably since the first fit. seven years ago. The acuter 
symptoms came on three years ago. 

Causation .—Congenital syphilis. 

Diagnosis .—General paralysis of the insane; (1) Progressive dementia; 
(2) Progressive paralysis; (3) Inco-ordination, tremors, &c.; (4) Speech 
(5) Abnormal pupils. 

I saw this patient on February 15. She was lying in bed, fearfully 
emaciated—legs drawn up with contracture. Pupils dilated, left a little 
larger than right, inactive to light. Speech —She seldom speaks, and 
when she does it is quite incoherent and unintelligible. Continually 
moans and mutters in an incoherent manner. She has difficulty in 
swallowing, but does not refuse her food. Passes everything under her. 

December 14, 1898.—There is now very definite ptosis. 

February 12, 1899.—The patient has become much paler and thinner. 
She is quieter, more demented, and cannot utter a sound which could be 
called articulate. She keeps her right hand over her mouth, and, if 
spoken to, gesticulates with her left, in which she appears to have more 
power. There is much more rigidity in the legs and pain on movement 
of legs and body. More sores over the bony prominences are developing. 
She exhales a bad odour. Physical signs reveal commencing (?) disease 
of the lungs. 

February 18, 1899.—Is paler still, and has a degree of emaciation 
which would appear to be almost incompatible with life. The skin is 
drawn tightly over the face, nose pen-shaped, eyes sunken, the lips atro¬ 
phied, and the teeth exposed and covered with the right hand. This may 
be due to the cold air giving pain on passing over the teeth, which are 
much decayed. Is very quiet and tends to sleep. Is practically in a 
condition of amentia, and leads a vegetable existence. If disturbed, 
makes a curious, querulous, wailing noise. This is accompanied by 
slight distortion of the features. Speech absolutely gone. Does not 
grind her teeth much now. 

Pupils. —Right medium in size, immobile ; left dilated, immobile. 

Legs. —Extensor muscles extremely atrophied; flexors also, but not 
quite so much as the extensors. Knee-jerks absent, as a result of 
muscular wasting. A jerk can still be obtained on striking the tendo 
Achilles and some of the flexor muscles. The knees are flexed, also the 
hips, resulting in the legs being drawn up. They are laid to the right 
side of the bed. They are quite paralysed and nearly rigid. Does not 
appear to feel pin pricks. Sores on sacrum trochanters, iliac crests, and 
on the inner side of the right leg, just above the knee. Arms much 
wasted, and reflexes cannot be obtained. There is not much rigidity, and 
there appears to be more movement in the left arm than in the right. 
Movements are very tremulous. Examination of lungs reveals scattered 
areas of tubular breathing, and in other parts low bronchial breathing. 
Phthisis (?). 


February 21. 1898*—Appear a to be dym#; friends sunbnDned once 
imu*. : :. ' O-V*-''/ ' "" • ’ v ; 

r*hnmy 22, 18VS9.—Died at 5.10 >«.uk 

X ii w mriebtt*# it* Dr. Lord for the sscellhnl finical note* of this case* 
h'Jowy (eight hynn'H ’ivffor death).— The body wa H extremely ema¬ 
ciated; GOf^weHcang Dub *vme -‘rigid ■ t£s(n&wl J>,atur&SmuSl parch¬ 
ment jjteawante#*.; sloughing area* over *acr un, trdcJiantierjs/iUac'crests, 
and inner eta Af n«>ht ta.o above kn*>.»; taha ttaved at. the kn^fiA and at 

pr^ciit. / fan<1 -0i<(Yu0<uii from- 6 to 8 mm, Duck ; mtevfrorifcai and 



Photograph £ oT thy two hemispheres cut horizontally ih nearly same 
situation, tV*mar‘fee 4 fcirhphy bf the left and thu dilatation of its latyml 
ventricle ie very^obvioits, jleduwl■£. 

coronal sutures- Were, -iti&rJttsil ’b.V.'oxtrcniely noticeable ridged externally, 
and internally hy ^ broad line of compact bone f dtt area over right 
frontal ^minerne >0iuo\vhat, thicker tb&ri the rent. Dm* t 

rmuatiafly adherent-- t-0*. ; longUudi&oj' status empty* Otj&fttf; 



excess of fluid. Weights (after draining)—Whole brain, 36 oz.; cere¬ 
bellum, pons, and medulla, 5 oz.; left hemisphere, 18 oz. = 367 grms. ; 
right hemisphere, 14f oz. -- 417 grms. Pia arachnoid —Markedly thickened 
over both hemispheres, especially the left, distribution being over the 
frontal and central convolutions, especially about the fissure of Sylvius: 
the occipital and temporal lobes, and the calloso-marginal convolution 
were comparatively little affected. All the convolutions in the regions 
of the thickened membranes were markedly atrophied. Ventricles were 
dilated, especially the left lateral (vide photo. 1, p. 297), and granulations 
were present but not marked. Substance of brain was soft and watery. 
Veins were not very congested, but the small vessels of the pia were more 
congested than usual, especially over the parts where the lepto-meningeal 
thickening was not marked. Stripping the membranes caused marked 
erosion of the cortex. On section the cortical grey matter was seen to be 
wasted, and its superficial striae lost. Vessels at the base were normal 
in arrangement and texture. Lepto-ineninges at the base were thick¬ 
ened and infiltrated. Cerebellum was soft. On section of the medulla 
the pyramids appeared wasted. The fourth ventricle was granular. 
Thorax —Both pleurae were adherent. Right lung weighed 12 oz.; con¬ 
solidation at the apex and upper part of lower lobe; broncho-pneumonia. 
Posterior part of lower lobe in a state of hypostatic pneumonia. Left lung 
weighed 7$ oz.; patches of grey hepatisation (broncho-pneumonic) were 
present, varying from a pea to a chestnut in size. Bronchial glands 
slightly enlarged. Heart weighed 4 oz.; there were no pericardial 
adhesions, a little pericardial fluid ; an agony clot present ; valves 
normal; muscle substance rather pale, but firm. Slight atheroma of 
aorta, both ascending and descending. Liver weighed 28$ oz.; a little 
stellate scarring on its under-surface, especially on the left side. On 
section, greasy and obviously fatty. Spleen weighed 2 oz. normal. 
Supra-renal capsules normal. Left kidney weighed 4 oz.; cortex pale, 
pyramids normal, capsules not adherent. Right the same, but weighed 
8 oz. Peritoneum normal. Pancreas normal. Alimentary canal normal. 
Uterus and its appendanges only weighed j oz.; slight erosion of the 
os uteri; ovaries extremely small, and no obvious Graafian follicles 
present.—F. W. M. 

Microscopical Examination. 

Top of ascending frontal by Nissl method shows a 
marked atrophy and disappearance of the cells ; those that 
are still left are in a state of decay ; they stain uniformly or 
imperfectly ; the Nissl granules are absent; the apical 
processes of the pyramidal cells are corkscrew-like and 
stained a dull purple. The second and third divisions of the 
dendrons are seldom seen, and the network of Gerlach 
appears atrophied, for numerous holes are seen. Sections 
show that the normal close meshwork of delicate fibrils 

•fvv'r.'vr^-.-T.-woue .»rvfe;NU.E -oksecai. 

altered/awing to atrophy of the cfendi'Me Uritfy 

phottttfticro. ,10. p, 5.MJK1). - 

-i i i l' .1 1 t 

Examination _*-#f the jwtetinn of the frontal and 

:' .</■£ ■'.■•: V“ • ; -V * VI ' . ’ ‘^A 7 ’-• '/’VlrV • • _ 'a. ' f . /• ' d t ll ' !> . 1 '. . 7- ■ ' *' 1 ' V.‘ jfl .1 !' ■* 

; • ’ >•* •.• v 

t»» ■>•.•: •• w 

There is ivry marked > i tiuloi atrophy in tbt- givy matter of 
ii*>t;h evr(voluttons. ljuf in the sitnution referred to there is> 
<■• iiwpleteiJcstnfctioir; there are seen, however, a number of 

(vide fig. ;V». "No Ot.nyetvtiui fibres are seen in the eorteK 

■' r -,y. 1 // 0 *.iyw /». 

. 300 . vHt'HIVfty •/ V.. ... ^ ;, 

at all. The corresponding -portion of the rj.g^|iS6JlU«pU¥:WJ- 
shows *><uisderahk* . infl&iijjn&tory pia .arachnoid;tbkk§hihg 
an*] some, odiuia;i- atrophy, especially of thti superficial 
layers, but it 1 - -intunisidehthle' as compared vvifcti the left. 

The iidlanihiafftty put affect)and the iny. , 

(lamiaat<>yy changes around the i?h^thy«Ssete are m direct 




• « 


R.>* * » J 




4 . : ' 

Pbotomiarogrfiplift 10, itecliair of lop ol a^ioditig fr^ntal,lfcffc homtepherti 
ataihod by Nittel method, sbvwifi^ ftto^Iry of Ktiparfieia^ /layers of~c*Ite vj. ■£/ :' ■: 

fispoc?aJIy>* without glia chIJ •proHfiomtiim, t-owpard with jert»h*T %o?y from 
normal brain. Magnification salX) difemetw. 


proportion to the *atropby on the t\vu sides. Possibly, iu 
this region the inflammatory changes are more marked than 
in the pHiaeoatrai lobule, because of the larger amount of 


cerebro-spinal fluid in this situation. There is a more 
marked proliferation of glia cells in the subjacent white 
matter of the left side as compared with the right. 

Fig. 1. 

The ova stained by Marchi fluid, showing black granules in the nucleus. 
Magnification 150 diameters. 

Fig. 2. 

An ovum (immature) more highly magnified, showing the black granules 
in the nucleus. Magnification 400 diameters. 

Fig. 3. 

Pyramidal cells stained black by Marchi fluid. Magnification 150 

Organs. Stained by Marchi Fluid. (Sections Cut in 


Ovary .—Stained by Marchi method. The immature 
ova are seen in abundance under a low power ; they are 
recognisable by appearing as clear spheres ; in the centre 
usually, but not always, are seen several granules which are 
stained black by the osmic acid. These black granules 
appear to be in the nucleus in many instances when 



examined under a high power. No Graafian follicles were 
observed in the sections. 

Heart-muscle. —The fibres are very attenuated ; striation 
very indistinct; nuclei granular brown pigmentation. Little 
or no fat granules seen after staining by osmic acid. The 
indistinctness of striation of the muscle-fibres is very 

Quadriceps extensor .—The muscle-fibres are attenuated, 
opaque and the striae either indistinct or quite lost. Some 
few, however, appear to have normal striae. There are no 
black granules in the fibres. 

Kidney .—There is a considerable amount of fat granules 
seen in the epithelium of the tubules of the cortex, especially 
of the convoluted tubules. There is increase of fibrous 

Medulla and 2nd lumbar segment of spinal cord .— 
Sections cut and stained by carmine and carmine-Weigert 
after embedding in celloidin. 

There was marked bulbar lepto-meningitis and atrophy 
of cells in the floor of the 4th ventricle. 

The spinal-cord sections showed slight lepto-meningitis, 
general overgrowth of glia cells in grey matter and central 
canal. Degeneration of crossed pyramidal tracts of both 
sides, more marked on the right. 

Case 2. 

C. V., aged 19, admitted into Claybury Asylum, December 21, 1894. 

On admission patient was found to be a childish, undeveloped-looking 
girl of 19, with a pale greasy-looking skin, dark straight hair and brown 
eyes. Her height was 4 ft. 10 ins., and her weight 8 st. She was well 
nourished, though not fat. Her chest was examined and nothing 
abnormal found. The breasts were also undeveloped. Her palate was 
very high and narrow, and the enamel of her teeth was lined transversely 
though their general shape was good. When she spoke, which was 
rarely and not spontaneously, there was hesitation and drawling. Her 
gait was shambling and she dragged her feet, being liable to trip. The 
knee-jerks were exaggerated, and the pupils regular and reacted. 

Mentally .—She is noted as having an imbecile appearance, and being 
simple and childish in manner. She is very confused and stupid and can 
hardly be got to answer questions at all. She does not know how long 
she has been here, but can count and multiply simple numbers. She 
cannot tell what day it is without long thought, and takes very little 


notice of what goes on around her. Emotionally she is indifferent and 
placid rather than happy when left alone, but when interferred with she 
is spiteful and now and then screams at the top of her voice, though as 
a rule she is quiet. Possibly the screaming may be due to headache. 
She has no delusions, as far as can be made out. 

Her past history, as got from her parents, is that she was healthy as 
a baby, had no rash or skin disease except the rash of measles, nor had 
she ever anything wrong with her eyes. She got over teething well with 
the help of teething powders, and had no convulsions. At school she 
seemed fairly bright, and was a jolly, cheerful girl. About 14 or so she 
left school and took a place as a servant, where she w r as w orked hard, 
and only stayed three months, because she felt very much overdone. 
Soon after she took another place, and in four months, because she waB 
top ill to stay, she came home. She was dull, and could not walk as well 
as usual. When at home she had a fit (then 16), after which she was in 
bed and had to be taken to the infirmary, where she was kept about four 
or five weeks. Subsequently her walking and her dulness became worse. 
She complained a good deal at times of pain in her left arm, which she 
used to rub, and also of some difficulty in swallowing. Her speech was 
noticed to be peculiar about one year before admission (i.c., at 18). Her 
character was quite altered; she became sullen and lazy, and stayed 
constantly in bed and took no notice of anything. Her habits were 
indifferent, and at last her parents were obliged to send her back to the 
infirmary and she then came to the asylum. She was always a steady 
girl, and had no worry, as far as her mother knows. She had never 
menstruated at all. 

Family history .—A grandfather and two uncles died of consumption. 
Father, who is alternately a coster and gas worker, is said to take too 
much alcohol at times, but no real history of alcoholism could be got. 
His wife states that only on rare occasions, when out for a “ spree,” had 
she seen him the worse for drink, and as a rule he was quite steady and 
had never been “gay” in any way. Moreover, the house is very 
comfortable, and he himself a spare athletic healthy-looking man who is 
“never ill.” 

Mother a charwoman, looks robust and says she has never had a day’s 
illness that she can remember, except her confinements, and that they 
were alw r ays easy and natural, with no trouble afterw ards. No definite 
syphilitic history in either parent was got nor any of nervous trouble. 
The mother had ten pregnancies, all full term, and no miscarriages. 
(1) The baby died in a week of so after birth, cause unknown. (2) The 
baby died wdthin six weeks of birth, cause also unknown. (8) Was the 
patient. (4) A girl, now 21, in service and healthy. The other six are 
all alive and well. She states that their teeth are good, as far as she 
knows, that they have none of them suffered from any nervous trouble, 
and have had only ordinary childish ailments. There are in all nine girls 
and one boy. 

Patient was admitted into the asylum at 19. During the first five 
months there is nothing very special to note. She got somewhat worse, 
suffered from frequent headaches, and during the last three her habits 



were bad; the bladder acting often, and the rectum occasionally, without 
her being apparently aware of it. In June, the sixth month of her stay, 
she had her first seizure since admission, and in the early part of July two 
more. They were slight, more like sensations, the nurses said, but were 
succeeded by a stuporose condition, and patient had to lie down for a 
long time after them. There was little or no spasmodic movement. 
Her habits during June and July, when she had the attacks, were very 
considerably better than during the preceding three months, when she 
had none, both as regards the bladder and the rectum. Her mental con¬ 
dition during this time remained much as described in the beginning but 
that she was possibly more dull and vacant. On July 27 patient had a 
severe seizure. She was quite comatose, with flushed face and dilated 
pupils, which were equal and insensitive to light. The pulse was 120, 
full and bounding, and the temperature 104*2°. There was some twitch¬ 
ing of the muscles of the left side, both limbs and face, and apparent 
paralysis of the right side, with some general rigidity. Knee-jerks exag¬ 
gerated. There was also retention of urine, and the catheter had to 
be used. Her bowels were constipated, and patient was given an 

July 28.—Next day temperature rose to 104*8° ; there was still reten¬ 
tion of urine and constipation, and patient was given calomel. 

July 29.—Patient began to menstruate for the first time, but scantily, 
and at once began to improve. Her temperature began to come down. 
The pulse was 88; respirations 24. Coma going off, and the paralysis 
less complete. There were red marks, from vaso-motor dilatation, on all 
points of pressure. Her chest was examined and nothing abnormal 
found. Bowels open five times. 

July 81.—She can draw up right leg and foot, but does not move right 
hand or arm. She is conscious to a certain extent. Temperature 100*6°. 

August 1.—Better. Pulse 96, respirations 18, temperature 99*8°. 
Menstruation stopped. 

August 2.—Takes more notice, and now, for the first time, the pupils 
are noticed to be unequal, the right being larger than the left, and 

August 4.—Patient is not so well, groaning slightly, duller again, and 
her breathing is shallow and hurried, with well-marked friction sounds at 
the base of the left lung in axilla. Pulse 120, respirations 86, tem¬ 
perature 99*2°. 

August 5.—Pulse 116, respirations 40. Friction can be heard nearly 
all over left side. 

August 6.—Some dulness on left side at base ; less friction. Pulse 
140, respirations 86. Almost comatose again. 

Got gradually worse. Difficulty in making her sw'allow; and she died 
on the 10th. 

Post-mortem notes .—Skull thick and dense, and dura mater very 
firmly adherent over whole surface. Dura mater much thickened. 
Superior longitudinal sinus dilated. Pia arachnoid much thickened and 
adherent to convolutions, especially over frontal region. When stripped 
off it left a worm-eaten looking surface. Cerebro-spinal fluid in great 


excess, and opaque. Cerebrum badly developed and small. Grey matter 
fair in amount, but gelatinous in appearance. White matter much con¬ 
gested. Lateral ventricles dilated, and the floor granular in places. Basal 
ganglia normal. Cerebellum normal. Fourth ventricle very granular all 
over. Spinal cord much congested. Heart small, with pale muscle and 
ante-mortem clots in the right side; valves healthy. Lungs not adherent 
to chest wall, but in the lower lobes of both, at the posterior extremity, 
there was an infarct, 2} in. at its base ; that on the right 1 in. Rest of 
the lungs were congested. Liver, spleen, and kidneys normal. 

This case was published in the Journal of Mental Science , by Dr. 
Helen Boyle. It proves to my mind neither the presence of syphilis or 
its absence in the father. The two first children dying so soon after birth 
is suggestive, although by no means presumptive of syphilis. The fact, 
however, that the man now appears healthy goes for nothing. 

Case 3. 

E. B., female, aged 14, admitted to Darenth Asylum for Idiots, 
December 8, 1896. 

History from mother .—The child was born at full time, labour normal. 
The father died of phthisis. The mother is alive, aged 84. Parents 
married when 20 years of age. Symptoms of mental disorder first 
noticed when she was 12} years old. She has become quite helpless 
and demented. (1) Miscarriage. (2) Miscarriage. (8) Child (boy) bom 
at full time, lived 15 months, died in convulsions. (4) Patient, labour 
natural; at seven years of age all her hair came out; she never had a 
tit. (5) The next child, a girl, is blind, both comese opaque (like opal). 

Two children have died of meningitis, aged respectively 10 months 
and 7 months. Mother always healthy up to time of marriage, 
afterwards she suffered from sore throat, and her hair came out. No 
direct or collateral history of insanity either side. 

I am indebted to my friend Dr. F. R. P. Taylor for these excellent 
notes and for calling my attention to this case, of which I took the 
following notes:— 

May, 1899.—She is lying in bed, with legs drawn up from contracture, 
knees and hips flexed. There is great muscular wasting, and the deep 
reflexes are markedly exaggerated. Both patellar, tricep and wrist tap 
contraction are readily obtained. She appears to have no power to move 
the legs, but can put her hand to her face. She has more power in the 
right hand than the left, or she uses it more. She does not respond to 
the calls of nature, and passes everything under her. She is quite 
speechless, and never utters any coherent sounds. The dementia has 
much increased, for she does not now recognise her friends. Lately the 
attendant informs me she has had considerable difficulty in swallowing. 
The pupils are equal, but react sluggishly to light, medium size. She 
apparently feels when pricked with a pin. She has never menstruated. 
She has had several syncopal attacks. 

The mother brought the sister of E. B. to see me at Charing Cross 




Hospital. She was suffering with very severe cyclitis and interstitial 
keratitis, and I obtained her admission into the Westminster Ophthalmic 
Hospital under Mr. Griffiths. I found that she had characteristic 
Hutchinson’8 teeth and slight linear cicatrices at the angles of mouth. 

Post-mortem (thirty-six hours after death)—June 10,1899—Body very 
emaciated, large bedsore size of crown piece over left trochanter, small 
bedsores over left trochanter audiliac crest. Post-mortem rigidity had 
passed off. Contracture of knees. Bladder distended up to umbilicus. 
Muscles a fair colour considering the emaciation. Left lung —15 ozs.; 
adherent to chest wall, adhesions break down easily. Congested and 
oedematous, floats in water. Bronchi filled with frothy mucus. Lung on 
section presents the appearance of broncho-pneumonia. Right lung — 
18J ozs., in the same condition as left. Skull —Intraparietal and frontal 
ridges well marked. Dura mater adherent. Great excess of cerebro¬ 
spinal fluid. Great thickening of pia arachnoid with opacity over nearly 
the whole of the hemispheres. Cerebellum and pons —118*2 grammes. 
Right hemisphere —846*7 grammes. Left hemisphere —818*4 grammes. 
Ventricles —Both lateral ventricles enormously dilated and granular; 
pia arachnoid greatly thickened and opalescent along upper border of 
mesial surface as far as occipital lobe and over the whole of the frontal 
and central convolutions. Parts which have to some extent escaped are 
the under surface of brain, especially the orbital lobes and whole of 
tempero-sphenoidal lobes. Heart —4$ ozs.; substance friable and pale, 
valves all healthy. Spleen —Soft, otherwise normal, 4$ ozs. Liver — 
92 ozs.; soft and fatty. Uterus and ovaries very small. 

Case 4. 

M. W., aged 28, single, but has one child. Admitted into Claybury 
October 15, 1896, died March 22, 1897; occupation, charwoman. 

On admission patient was found to be a short, brown-haired girl. 
Height, 4 ft. 11 in.; weight, 8st. 7 lb. She had a sore on her right 
buttock. The lungs and chest were examined and nothing abnormal 
was found. The breasts* were large. The pulse was 84, regular and of 
good volume. The tongue was furred, moist and tremulous. She had 
Hutchinson’s teeth and a high palate. The bridge of the nose is 
depressed . Her appetite was bad and her bowels confined. Her sight 
was good and her pupils were regular and reacted to light and to 
accommodation. Her senses were fair *, muscular power and gait were 
good. Patella reflexes were much exaggerated. Mentally she is imbecile 
in manner and appearance and when spoken to laughs in a silly, childish 
way and w*ill not answer a question. She has very dirty habits and 
does not seem to understand what she is doing. She is restless and 

Family history .—The mother states that there is no consumption, 
insanity, or alcoholism nor any history of tits in the family. 

Past history, —Patient has never had an attack of insanity before and 


this one came on after her confinement a month ago. She is of ft 
cheerful disposition but has had great trouble, having been deceived by a 
young man. With regard to alcohol, she is steady and she has never 
shown suicidal tendencies. 

October 22.—Patient is suffering from puerperal mania. She is 
extremely restless, noisy, sleepless and excited. She throws herself 
about and is in a padded room. She refuses to reply to questions, is 
resistive, hysterical, shaky and trembling and indifferent as to habits 
and to her food. There is an indistinct cardiac apical murmur and she 
is in impaired health and condition.—R. J. 

October 29.—Patient is vacant and confused, restless with choreiform 
movements, wet and dirty and everything has to be done for her. She 
takes food indifferently, sleeps poorly, is cyanosed and has a feeble 
heart. Her reflexes are very much exaggerated. Her speech is slurred, 
and she is happy and says she is very well.—T. K. S. 

November 5.—Patient improved with a cardiac tonic. She is quieter, 
less fidgetty and not now destructive. She eats and sleeps better. 

December 18.—Patient is in bed with right basal pneumonia. She is 

January 11.—The pneumonia has cleared up. There is now pain 
over the liver and pain (probablv referred) in the right iliac region.— 
T. K. S. 

February 9.—There is phthisis of the apex of the left lung and the 
diaphragmatic pleurisy which appeared extended to the left side and over 
the lung. Patient is very feeble. 

March 9.—There is a cavity at the apex of the left lung ; the whole 
lung is breaking down and the patient is very cyanosed and sits up in 

March 22.—She became gradually worse and died to-day.—T. K. S. 

Post-mortem. — Post-mortem about fifteen hours after death. State 
of nutrition fair. Post-mortem rigidity not present. There was a slight 
abrasion of the skin on the right buttock, Depressed bridge of nose and 
syphilitic teeth. The skull was symmetrical, thick and dense. The 
dura mater was adherent to calvarium in frontal region. There was 
excess of fluid in subdural space. The pia arachnoid was opaque and 
thickened. Erosions of cortex of first frontal on either side. Excess of 
fluid in subarachnoid space. The brain weighed 89J oz. There was 
some congestion. The convolutions were simple, large, and sulci wide. 
Cortex soft; upper layer easily detached; small in amount. White 
matter soft; punct® numerous. Some oedema. Left lateral ventrical 
larger than right . Choroid cystic. Floor granular. Cerebellum weighed 
5 oz.; congested. Pons and medulla soft and congested. Right pleura 
obliterated with recent adhesions in lower half. New'ly organised ad¬ 
hesions over whole lung. Bronchi congested ; bronchial glands enlarged 
and pigmented. Lungs were both congested and studded with tubercular 
masses. In a few small places these masses had become confluent and 
cavity formation was commencing. Heart weighed 10 oz.; valves 
slightly thickened. Muscular tissue soft, friable ; coronary arteries patent. 
Some slight atheroma of aorta. Peritoneum riddled with tubercular 



deposits. Liver weighed 61 oz. ; large ; cirrhotic; firm in appearance ; 
yellowish in colour ; studded with small gelatinous points of tubercule. 
Spleen weighed 8 oz.; studded with caseating tubercule. Kidneys each 
weighed 4J ozs. Abdominal glands enormously enlarged and caseous. 
In the position of the foramen of Winslow was a large mass of caseating 
glands about the size of a small hen’s egg. Bladder contracted and 

Cause of death .— General tuberculosis. Congenital syphilis. General 
paralysis.—E. K. Stansfield. 

Cane 5. 

M. B., aged 20, single ; occupation, stringer. Admitted, April 9, 189'). 
Died, May 8, 1895. 

On admission the patient was found to be a fairly-nourished girl, with 
brown hail*. Height, 5 ft. 2 in.; weight, 8 st. Her tongue was clean, 
the palate fair, and her teeth were small, with the upper incisors notched. 
She rolls about in walking, but her muscular power is fair. She is too 
noisy and restless to examine thoroughly. 

Mentally .—She is exceedingly noisy and restless, constantly throws 
herself about, and laughs and shouts. Her answers are incoherent. 
Before admission she is noted in the certificate as follows:—“She 
says she is followed about all day and night by men and women. She 
hears marriage bells and voices in America calling her. She sees strange 
people in the room at night.” 

Family history .—A great-grandfather was insane. 

Past history .—She has suffered from pains in the head and has been 
much worried by want of work ; the latter is assigned as the probable 
cause of this attack. She has never been insane before, and has only 
been noticed to be so for the last three weeks. 

April 18.— Patient is suffering from mania. She is noisy and excitable 
and erotic. Is shamefaced and coy, will not answer questions, refuses to 
give particulars of herself, will suddenly shout out tirades against every¬ 
one in general; sings and behaves in an uncontrollable manner. She is 
in fair health and good condition, and looks more than her age. 

April 25.—Patient is very restless and troublesome. She throws 
herself about and has erotic manners. She eats and sleeps well. 

April 27.—She is quieter and more staid. Clean in her habits. 

May 8.—Patient is inclined to be restless and troublesome. Dirty and 
of wild appearance. 

May 5.—She was very noisy and restless two nights ago, and threw 
herself about. She was exhausted in the morning. She took food fairly 
the next day. To-day there is distension of the abdomen, and pain. The 
abdomen is tympanitic all over. The bowels are not open, and a glycerine 
enema was given, with no result. A fomentation was applied to the 
abdomen, and tinct. opii., Ill xv., given by the mouth. The bed was wet 
and slightly stained with dirty brown discharge. The catheter was 
passed, but nothing came away. 


May 7.—To-day patient is very collapsed, lies on her back, and the 
abdomen is distended and dull on percussion, except in the region near 
the umbilicus. The catheter was passed, and two ounces of brown, 
slightly-turbid urine drawn off, She takes nourishment well, and there 
is no pain or tenderness. The pulse is wiry. 

May 8. —She gradually sank, and died of syncope.—H. Boyle. 

Post-mortem .—The cause of death was found to be general paralysis. 
Ruptured bladder. Both ovaries were collections of cysts. 

Case 6. 

S. S., aged 22, admitted into Colney Hatch June 9, 1897 ; domestic 
servant. Tongue very tremulous. No friends or relations. Father and 
mother dead; brought up by Sisters of Mercy. No history obtainable. 
Seizures. Anxious expression. Pupils equal, react sluggishly. Knee- 
jerks absent. Lost consciousness a few days ago. (? General paralysis 
of the insane.) Since been up. • 

July 13, 1898.—Now in bed ; helpless and speechless; tries to put out 
tongue, which is very tremulous. 

August 17, 1898.—Speech very characteristic of general paralysis of 
the insane, tremulous, syllabic, tongue tremulous. Pupils unequal, react 
sluggishly to light. Tremor in the hands. Every now and then has 
congestive seizures and becomes helpless, and sits in a chair. Used to 
work in laundry. Does not know for certain whether it is summer or 
winter. She is able to swallow. No signs of congenital syphilis upon 
face, except perhaps central incisors slightly pegged shape. Knee-jerks 
absent, sways a little with eyes shut. Can tell the time within five 
minutes. Before admission was in service in the Mile End Road, and 
before that was taken care of by Sisters of Mercy. Says that father and 
mother’ both died quite young. Probably an illegitimate child. No 

September 17, 1898.—Pupils equal, sluggish reaction to light, react 
well to accommodation. Marked tremor in face muscles on showing the 
teeth. She has defective knowledge of time and place and is now quite 
childish, although she was able to pass the fifth standard at school. 
There is a marked loss of expression in the face and tremor in the hands. 
She has not menstruated since she has been in the asylum. She is fairly 
well nourished. Knee-jerks not obtained. Can feel the prick of a needle. 
She has had two seizures since I saw her last, when the temperature went 
up to 100° in one of them.—F. W. M. 

November 5.—Pupils unequal, sluggish reaction to light; tongue very 
tremulous and jerky. When asked to write her name wrote four times a 
very shaky letter “ S,” but she was unable to get beyond this. The 
tremor and inco-ordination increased with each effort that she made. 
There is well marked wrist tap contraction on the right side, and a slight 
contraction on the left. The legs are well nourished and muscular. The 
plantar reflexes are rather exaggerated. Knee-jerks not obtainable, 
sensation is apparently normal in the legs. She has had no seizures 
lately, but latterly she has been obliged to keep to her bed. Her memory 
is bad. Temperature is 97*6°. 



November 19,1898.—Arterial pressure 125. Pulse very small. Heart 
sounds, first muffled; second accentuated. She is tatooed on the right 
arm; this she says was done by her young man who was in the Royal 
Marines. She says she did not live with him, but she gave him up 
because he drank so heavily. Temp. R. 96*8°, L. 96*8°. She is now 
quite recovered from the seizures, and looks and feels much better. 
She walks with rather a wide base, coming down on her heels first. 
Knee-jerks absent. 

June, 1899.—The patient is more feeble and demented. 

Case 7. 

J. A. C., admitted into Colney Hatch September, 1896, suffering from 
imbecility; aged 22. 

The following note was made .—Bodily condition fair. Head rather 
large. Pupils equal; react to light and accommodation. Thoracic, 
abdominal, and genito-urinary systems apparently normal. Mental 
state dull and weak-minded, intelligence impaired. She has the delusion 
that she is being followed about by a man in woman’s clothes. 

January 7, 1897.—There is the characteristic slurred and hesitating 
speech, with a fine tremor of the tongue on protrusion. Pupils are 
equal but dilated, and react sluggishly to light and to accommodation. 
Knee-jerks are both very exaggerated, and she is slightly unstable on her 
legs, and walks on her heels. She is well nourished, inclining to be 
stout, but her general health is distinctly impaired. She considers her¬ 
self well and strong. She says that her father, who is a wood-cutter, has 
given up work for some time, being completely paralysed. She lias a 
sister in Leavesden Asylum, who is blind. She says that she has been 
ill-treated and knocked about by her stepmother. She is willing and able 
to do a little work in the ward. She appears to have had no fit or seizure 
up to the present time. She cannot write her name.—F. W. M. 

April 22, 1897.—General paralysis is advancing, and she has been less 
able to work of late. Is very stout, with much impaired health. More 

June 5.—Is now capable of very little work. Has very characteristic 
speech. Is happy and contented. Pupils equal but always dilated. 
Mouth drawn to the right side. Tongue very tremulous. Knee-jerks 
exaggerated. Very incoherent. 

July 15.—Tried to make a straight line with pencil on paper, but with 
difficulty made only a very crooked one. Getting more tremulous and 
demented. Pupils are a little unequal. There is sluggish reaction to 
light and to accommodation.—F. W. M. 

August 25.—Very seldom able to do any form of work ; very stout, 
very feeble, very tremulous. 

September 29.—For the last week patient has been quite powerless, 
unable to stand, lies in bed like a log. Is quite unintelligible in her 
utterances. There has been no seizure. 

October 17.— Her brother (a road labourer, and who has the same 


dreamy expression as patient and talks in a slow, drawling manner, much 
as she does, and from his manner of speaking shows clear evidence of 
feeble mental powers) has visited her. He states that his father has been 
a firewood-cutter, but is now in Highgate Infirmary, with paralysis. He 
has been a cripple ever since he was a boy. He is married for the second 
time. By the first wife he had Bix children. Besides patient there are 
four girls. Two of these died young. One is married, and the other is 
now in Hanwell Infirmary. She went there from Highgate, and was 
previously in Leavesden Schools. This sister has bad eyes, and her sight 
is much affected. He was the only son (brother to patient). Father 
suffered from rheumatic gout a good deal, otherwise his health was good, 
and he was able to work. Mother died in St. Pancras of asthma and 
bronchitis. A male cousin on the mother's side was in an asylum. The 
patient of late has lived with her married sister. Her stepmother used 
to hit her, and she was “ clouted ” by her late mistress. She was of very 
hasty temper, was childish in her behaviour, and used to tell most atro¬ 
cious lies, such as telling people that her father was in prison, and her 
mother took her money out of the savings’ bank. Never had much 
schooling, and used to work at a laundry and in service; but used to 
complain and run away. Always seemed childish in her behaviour, play¬ 
ing with children and at childish games and with knives. He never knew 
her to have a fit. 

December 5.—Has been getting up for some weeks, but is quite lost 
and incapable of doing anything. She understands little that is said to 
her, and is quite unintelligible in her speech. She is faulty in her habits, 
and there is slight paresis on the right side of face. She walks on one 
side, with the right shoulder considerably lower than the left, but does 
not seem to drag either foot. Tongue and speech very tremulous. Does 
not seem to be able to protrude tongue. Both pupils widely dilated, but 
both equal; reaction to light absent. 

March 17,1898.—Has been in bed for some weeks. Is quite demented, 
hardly talks, simply smiles when spoken to. No control over sphincters. 
No seizure since last note. Helpless, but throws herself about. 

June 28.—Has not been out of bed since last note was made. Quite 
lost, incoherent, and hardly able to make an intelligible sound. No 
power over sphincters. 

September 11.—Patient has been visited by her father, a feeble old 
man; right leg drawn up and left arm contracted.—C. B. 

September 17.—The attendant says she has noticed frequent con¬ 
gestive seizures, but never convulsions. She has recently become 
much more helpless and has had difficulty in swallowing. She has lately 
been very destructive, continually tearing up her clothes. She has not 
menstruated since she has been in that ward (eighteen months). She 
recognised her father and brother when they came to see her. She does 
not talk now, although she will sometimes try to tell you her name. 
Temperature 99*6°. There is a marked tremor of the facial muscles and 
a bien itre expression. Dr. Beadles saw the brother and thought that he 
was somewhat similarly affected. 

September 18.—Her sensation is blunted over all parts of her body. 



Pupils equal and react sluggishly to light. All the facial muscles are 
constantly on the twitch; constantly mutters to herself, but is quite 

September 26.—Steadily becoming worse. For the last few days 
she has been in an extremely lost state ; would not make even a sound 
or take any notice of questions put to her. Very restless and constantly 
stripping herself. Has great difficulty in swallowing. Is on slop diet. 
Has had no distinct seizure since I treated her.—F. C. R. 

October 8.—Still continues in the same lost condition ; cannot speak, 
but occasionally shouts out. Has still a great difficulty in swallowing, 
Is not so restless, chiefly due to her exhausted condition. She has abed- 
sore on buttock and her legs very readily blister when they come in 
contact. Very wet and dirty. Has not menstruated while in the 

October 23.—Patient has been in more or less the same mental state 
as above note until to-day about 12 o’clock (midnight); I was called to 
see her; she was then in a semi-unconscious state. A weakness of 
right leg and arm. The nurse states that the right side kept on 
twitching (but that I did not see). The temperature under right arm 
was 100*4° and under left 99*6°. 

October 24.—This morning she has rallied somewhat; the weakness 
in the right arm and leg is not so pronounced ; sensation over the whole 
body very blunted. Cannot swallow any food whatever. Still has one 
or two bed-sores and has lost flesh rapidly of late. Temperature, 
evening, E. 100*2°, L, 99*2°. 

October 25.—She lies in a helpless, lost state ; appears to be partially 
unconscious. Cannot take any nourishment. Has had no more seizures. 
Evening temperature, R. 101*2°, L. 100.4°. 

October 26.—She has gradually sank into an unconscious state and 
died at 4.30 p.m. Morning temperature, R. 100*8°, L. 100*2°. 

The above notes are by Dr. Robinson. 

Family history .—Obtained from the father, C. C., aged 59, now 
an inmate of St. Pancras Workhouse Infirmary for paralysis. Up to 
three years ago his occupation was that of a wood-chopper. He has 
now left hemiplegia and is helpless, for, although he has recovered power 
on the left side of his body to a considerable extent, he is unable to get 
about, because of old hip-disease in the right leg. The attack of paralysis 
came on rather suddenly and he did not completely lose consciousness. 
His wife died twelve years ago, aged 36, of lung disease. She was a 
heavy drinker,, but there is no insanity in the family on either side, nor 
any nervousness, even such as epilepsy. The man himself used to drink. 
He denies having had syphilis, but says he had gonorrhoea. Family: 
First child, a girl, died aged 6 months; second a son, alive; third a 
miscarriage; fourth patient; fifth, a girl, alive, aged 22 ; sixth died at 
9 months; seventh, aged 16, at Leavesden School, now in service. At 
17 he tells me the patient went as a servant and seemed quite right. Up 
to three years ago was quite well and was bright and intelligent, but she 
never could read or write, as she never went to school. 

Post-mortem notes .—Post-mortem fourteen hours after death; body 


fairly well nourished. An old scar, about the size of a florin, on the 
middle of the right thigh. No other signs on the body which might in 
any way be considered as indicating syphilis. Rigor mortis passing off. 
Skull rather thicker than normal, the calvarium was heavy, and the bone 
dense. Dura mater not adherent. Small post-mortem clot in the 
longitudinal sinus. Large amount of fluid in the subarachnoid space. 
Thickening and opacity of the pia arachnoid over the-frontal and central 
convolutions with congestion of the veins opening into the longitudinal 
sinus. The pia arachnoid strips leaving erosions. Weight of the brain 
on removal and containing a certain amount of spinal fluid in the 
ventricles 32 oz. Weight of the separate parts:—Cerebellum 5J oz.; 
pons and medulla J oz; right hemisphere 12£ oz. = 360 grins.; left 
oz.=844 grms. Convolutions atrophied. Grey matter diminished 
in thickness, striation very indistinct or absent. Lateral ventricles 
dilated. Ependyma slightly granular. Ependyma fourth ventricle more 
obviously granular. Portions of top of ascending frontal. Broca’s con¬ 
volution, spinal cord, medulla, cerebellum preserved for microscopical 
examination. Thoracic and abdominal viscera —Right lung healthy, 
weight 14 oz.; left lung some hypostatic pneumonia of the base, otherwise 
healthy, weight 16 oz. Heart 8 oz. Valves healthy, muscle substance to 
the naked eye healthy. Liver 36 oz., apparently fatty. There are small 
yellow areas on the surface, which on section are found to penetrate into 
the substance of the organ to a short distance. The spleen weighs 2 oz. 
There is superficial thickening of the capsule of a nodular character over 
an area about the size of a florin. Does not appear to penetrate into the 
substance of the organ. Aorta —Throughout the whole surface of the 
descending aorta there are little yellow raised patches and streaks, 
especially round the orifices of the vessels (?) atheroma. Kidneys —Right 
31 oz.; left 4 oz.; congested and slightly fatty. Uterus —Small and ill 

developed. No hymen. Ovaries - Small capsule thickened, no sign of 
Graafian follicles. Portions of the organs described kept for examination. 

Microscopical Examination. 

Fatty change in periphery of lobules of liver marked. 
Fairly marked early fatty degenerative change in heart- 
muscle. Slight fatty change in convoluted tubules of 
cortex of kidney. 

Spinal cord .—Slight sclerosis in Goll’s tract and pyra¬ 
midal system of both sides and some recent degeneration 
shown by Marchi method in pyramidal systems of both sides. 
The 7th cervical spinal ganglia were examined, but no 
noteworthy change found. 

Cortex .—Ascending frontal and parietal :—(1) atrophy of 
tangential system by Marchi-Pal method ; (2) atrophy to a 



less degree of striae of Baillarger; (3) degeneration (recent) 
of a few large axons of pyramidal system demonstrated by 
Marchi method, and corresponding, therefore, probably 
with those fibres found degenerated in the cord. 

Cortex .—Nissl method. Paracentral lobule and Broca’s 
convolution. Atrophy of pyramidal cells. None show 
normal Nissl granules; most have deficiency in processes. 
There is a proliferation of glia cells. Dilatation of the peri¬ 
vascular lymphatics and cellular proliferation around the 
vessels. Sections through the medulla show some changes 
in the chromoplasm of the cells. On the floor of the 4th 
ventricle there are numerous granulations; these little 
elevations, about £ mm. to 1 mm. in transverse section, 
are apparently caused by a proliferation of glia cells and also 
dilatation of subjacent lymphatic spaces. Cerebellum .— 
The cells of Purkinje showed slight changes in the chroma¬ 
toplasm ; but otherwise were normal. 

Uterus .—Examination after staining in Marchi fluid 
showed normal epithelium lining the organ and the tubular 
glands; but in some places this epithelium showed fatty 

Ovaries .—Infantile in size. Bight ovary .—A number of 
sections cut in celloidin and stained with logwood and eosin 
showed absolutely no ova nor Graafian follicles. Left ovary 
showed only a very few ova, but there are one or two ripe 
Graafian follicles. 

Case 8. 

E. M., aged 26, Colney Hatch. 

I saw patient on September 8, and took the following notes :—She had 
been in Colney Hatch twice before, and was discharged each time as 
recovered. The history given to me by her father was as follows :—Up 
to three years and four months ago nothing verj’ noticeable had occurred 
in her conduct and habits to suggest the existence of any mental disease. 
About the time of her mother’s death, whom she had nursed for some 
time, it had been noticed that she was becoming strange in her character. 
She was not in the least put out by her mother’s death, and expressed 
not the slightest grief. The next thing her father noticed was she became 
enamoured of a young man, and set about the story that she was going 
to marry him. The Prince of Wales was coming to her wedding, and 
thousands of people. She ran her father into debt, and he was obliged 
to have her removed to the asylum. 


Family history .—Father formerly a seaman till he was 80, when he 
left the Royal Navy, and married. He had been in the way of getting 
syphilis, but to his knowledge had never had it. He has been in his 
present employment as a railway porter for twenty-nine years, and has 
enjoyed fairly good health. His wife died two years ago of cancer of the 
liver. There is no insanity, epilepsy, or nervous disease on either side, 
as far as he knows. His father died of phthisis. He has had six 
children. No miscarriages or still-births. The first child died at sixteen 
months, (?) measles. The patient was the second child, and was bora 
four months after the first died. The third alive and well, aged 24 ; the 
fourth well and fairly strong; the fifth, boy, died at 20, of phthisis ; the 
sixth, boy, alive and well. The patient, E. M., was a bright and intel¬ 
ligent girl, and passed the seventh standard at school, and went into 
service at 15, and up to three years ago remained in service ; she was a 
steady girl and a good daughter. No insanity or neuropathy in family 
on either side. 

September 8.—Present state :—Physical condition: height, 5 ft. 3 in.; 
well nourished. The face is flushed, slightly asymmetrical. There 
is opacity in the left cornea . Pupils dilated, and react neither to light 
nor to accommodation. The examination of the fundus: vessels normal 
in size, appearance of commencing grey atrophy of the disc. There 
is a marked tremor of the face muscles; the tongue is protruded in 
an irregular, jerky manner, and is tremulous. The teeth are small, 
but not of a syphilitic nature; one left upper central incisor carious; 
the teeth appear almost infantile in size. The palate is high, the 
nose rather broad, but not sunken. There are no rhagades around 
the mouth. The cervical glands are enlarged on the left side. The 
knee-jerks are exaggerated markedly. There is no appreciable loss of 
sensation. She has not menstruated regularly. Her writing is like her 
speech, tremulous. Thinks it is quite correct what she has written, thus 
showing her mental failure. Her speech is characteristic, syllabic, and 
tremulous. There is also a fine tremor in the hand observable. She has 
never had any fits, and her grasp is fairly strong in both hands. She 
does not respond to the calls of nature, and is accordingly wet and dirty. 
She knows where she is, telling me in Colney Hatch Asylum, where she 
has been twice before. She volunteered the remark that when she was 
here before she believed she was Queen Victoria, but she does not think 
she is now. She has a pleased, happy expression, hien etre , w r hen she is 
talking to you. She knows the time of the day and the day of the month, 
and I should say that her dementia is now not marked, for she could tell 
me most events that had happened in her previous life, remote and 
present, thus showing that her memory is still good. 

January 18, 1899.—Three months ago she became excited and 
maniacal, and this condition lasted for about six weeks. She then 
became as she is now, dull and stuporose, refusing ordinary food and 
never talking. Sits all day in a listless, apathetic state. Her face is 
flushed and cyanosed, likewise the hands. The skin is cold, and the 
pulse is so small as hardly to be felt. The knee-jerks are absent, and 
the muscles wasted. Nothing will make her take any notice of anything. 



February 4.—She died of asthenia and pneumonia of right upper lobe. 

Post-mortem notes . — Post-mortem thirty-six hours after death. 
Weather cold. Rigor mortis passing off. Body fairly nourished. Bed 
sores on both trochanters and sacrum. Small gangrenous eschars on 
both feet and on left great toe. Pupils dilated, equal 9 mm. Skull 
normal in thickness; adhesion of dura mater. Brain —Weighs 88J oz.; 
very congested veins all over hemispheres. Pia arachnoid thickened over 
frontal and central convolutions, and when stripped brain substance 
lacerated; substance very watery and soft. The only firm portions of 
the hemispheres are the occipital lobes. Weight of hemispheres are : 
Right, 15J oz.; left, 15* oz. Cerebellum, 5J oz.; ventricles dilated; 
very granular ependyma. Spinal cord infantile in size; much wasted; 
no naked-eye change. Thorax —Fluid in pericardium. Heart —6 oz.; 
normal valves and substance. Aorta —No atheroma. Lungs —Right, 
14J oz.; pneumonia; grey hepatisation of upper lobe. Liver —88J oz.; 
nutmeg. Kidneys —8£ oz. each ; rather greasy ; capsule strips. Spleen 
2J oz.; normal. Intestines —Normal. Bladder —Distended; no cystitis. 
Reproduction organs —No hymen ; vagina large ; ulceration of os uteri. 
Uterus small; ovaries small; soft. All organs taken for microscopical 

Cause of death —Pneumonia ; juvenile general paralysis of the insane. 


Microscopically, the brain showed the usual characters of general 
paralysis—absence of tangential fibres, atrophy of nerve cells, proliferation 
of glia cells, congestion of vessels, dilatation of perivascular lymphatics, 
also of pericellular spaces. Ovaries —Right ovary, no follicles' or ova 
found in sections ; left showed Graafian follicle and ova. 

Case 9. 


A girl, aged 24 on admission, single. 

She was the only child of parents whose age showed much disparity— 
the father being much older than the mother and he had all his life been 
a very hard drinker; he died aged 70. Her mother was nervous and 

Patient had keratitis when aged 7, and had been more or less under 
medical treatment since. From time to time she gave evidence of 
hysterical attacks. Three years before admission she had a great shock 
over a love affair and two days later was unconscious and remained so 
for three and a-half days, but talked incoherently all the time. During 
the following twelve months, tremors showed themselves and have 
persisted. On one occasion she wandered away from home for several 
days. She also had another unconscious period, during which there was 
much spasm of the left limbs; this followed upon some rather startling 
sight at the Zoo. For six weeks before admission to the National 


Hospital, Queen Square, she was very drowsy and she did not speak; 
date of admission to Queen Square was May 19, 1897. 

She had always been a very clever girl at artistic work,—could paint 
well, sing and play and had gained many medals, &c. 

Dr. Ferrier did not come to any definite diagnosis — hesitating 
between general paralysis and disseminated sclerosis. 

On admission to Banstead she showed distinct mental enfeeblement, 
was full of smiles and expression was slightly imbecile. She seemed very 
pleased with herself and evinced considerable bien etre . She only 
understood the simplest remarks and seemed unable to reply to many, 
frequently giving the answer “yes” in a meaningless way; she could 
barely stand, tended to fall backwards. Knee-jerks much exaggerated 
and slight ankle clonus. Well marked triceps reflex, pupils unequal, 
left the larger, did not respond to light or during accommodation. 
Discs normal, but retinal vessels seemed unusually sharply defined and 
somewhat narrow in calibre. No nystagmus or squint. Much tremor 
of limbs noticeable, this chiefly in arms and especially in hands and 
forearm, less so in trunk. Their presence depended on voluntary move¬ 
ment and ceased during sleep. Tongue protruded jerkily or not at all. 
Speech tremulous, but not quite characteristic of general paralysis, the 
quaver was from beginning to end and did not come on until towards 
the last few words. Palate of neurotic type. Breast tissues slight, 
but axillary and pubic hair plentiful. Temperature 99°. Pulse rapid, 
w f eak and rather irregular. Urine free from sugar and albumen. No 
fissures round mouth—one upper incisor had a slight notch in it, but she 
could not be said to have true Hutchinson's teeth. 

Her state varied, she w as mostly in bed ; occasionally was got up and 
once or twice was seen to walk or run across the ward, though at other 
times she could not stand. She was often very noisy and restless, 
tossing about the bed and often crying out as if in great pain. At 
times delirious, and then temperature was more raised, 100*5° and pulse 
sometimes nearly imperceptible. Nearly alw ays required to be fed with 
a nasal tube, occasionly took custard herself. Also twice required the 
catheter. Limbs show ed rapid wasting and a month after admission a 
trophic sore developed on buttock and another on the nape of the neck. 

At the end of three and a-half months she succumbed to an attack of 

My opinion of the case was that it was one of general paralysis, but I 
was not present at the autopsy and there was no microscopic examina¬ 
tion made, that I know' of. 

The skull-cap was of normal thickness but denser than usual and left 
side slightly smaller than right. Dura mater slightly thickened. Con¬ 
siderable excess of cerebro spinal fluid. Pia arachnoid thickened, and in 
frontal regions opaque and rather gelatinous; and there were typical 
adhesions round the Rolandic sulcus on each side. No atheroma of vessels. 
Weight of brain with some fluid in ventricles 1010 grms. Right hemi¬ 
sphere 420 grms. Left hemisphere 875 grms. Cerebellum 115 grms. Pons 
and medulla 15 grms. Hemispheres soft, considerable wasting of con¬ 
volutions. Generally pale. Lateral ventricle large, no granulations on 



ependyma. Ependyma of 4th ventricle had marked granulations. 
Myocardium pale and flabby. Commencing pneumonia at right base. 

Case 10. 

M. G., a single needle-woman, aged 17; height 4 ft. 9 in. Came to 
Dr. Head in the London Hospital on July 16, 1897. 

History. —Patient’s mother was a servant, and was married at 20. 
Her father was a dock labourer and was married at 22. Her mother is 
alive, and “ has not known what a day’s illness is.” No collateral insanity. 
Father died of an accident, aged 46. 

There were twelve children in the family, as follows:—(1) Dead, five 
months foetus; (2) Dead, five or six months foetus; (8) Dead, six or seven 
months foetus; (4) Dead, seven months foetus, lived eight hours; (5) 
Bom alive; living; 44 very delicate;” 44 ulcers on his legs;” “ inflammation 
of his eyes;” (6) Patient; (7) Girl, living, well, aged 16; (8) Boy, living, 
well, aged 14 ; (9) Boy, living, well, aged 12; (10) Boy, died of convulsions, 
teething and diarrhoea at 11 months; (11) Girl, died at 8 months, 
44 something the matter with her brain, and club foot;” (12) Boy, living, 
well, aged 7. 

Patient'8 history .—Patient has always been a delicate and fretful 
child, and required careful nursing from birth. She had snuffles and 
measles eight or nine years ago. She was vaccinated at four months. 
She always had a trembling on the left side, and that side became weaker 
and weaker until she was scarcely able to walk, and fell about at times to 
that side. 44 Her legs seemed to give under her.” She went to school 
between six and seven, and got on well. She seemed to pick up things 
so quickly that she passed the seventh standard at twelve years old. She 
was handy with her needle. After leaving school at puberty she became 
dull and melancholy, sitting by herself for hours and speaking to no one. 
At fourteen she began to menstruate. For a few months she was quite 
regular, and then the flow gradually ceased. There was no flow till three 
months ago, and then nothing since. Between 14 and 15 the left arm 
and leg 44 seemed always on the move.” Then her tongue seemed to 
be always on the move in and out of her mouth. Within the last two 
years she seems to have gone childish, and every day seems to be getting 
worse. For the last six months she has complained that her right hand 
has been on the twitch. She has always lisped a little, but for the last 
two years it has been getting very much worse. She complains of attacks 
(about every two or three days) of creeping pains beginning in the left 
hand, leg, side, head and tongue, “like rats gnawing.” These last 
sometimes an hour. She has had no fits, no fainting, no attacks in 
which she has become paralysed. 

Patient is a medium-sized, somewhat squat girl of 17. Her nose is 
broad and flat, with the bridge uniformly badly developed. Her mouth 
is broad with slight scars inside both angles. There is no extreme 
scarring. Her forehead is high and domed. The upper central incisors 
are notched, and the left upper molar sixth has four pointed cusps. On 
the right upper molar sixth this arrangement is less marked. Both lower 


molar sixths are decayed. There is no scarring on her body and her 
breasts are largely developed. Her speech is profoundly affected. The 
alteration in the speech consists of a slight slurring, an increase in fre¬ 
quency and length of the pauses and marked irregular glossal sounds, 
making her speech thick. Her writing is profoundly affected, especially 
when one considers that she has reached the seventh standard. She 
complain of occasional headache on the forehead This she says she 
often has. There appears to be some slight tenderness, but satisfactory 
examination is impossible. She does not vomit. She walks with con¬ 
siderable difficulty, and with marked unsteadiness, but does not fall with 
her eyes closed. There are marked irregular movements of her hands, 
but no true inco-ordination. She succeeds in touching the tip of her nose 
accurately with either hand. The muscles which move the fingers and 
the toes on the left side are in constant irregular movement. Not 
choreic and not fibrillary, but simply irregular contractions of the 
muscles exactly resembling those seen at the beginning of a Jacksonian 
fit or in a seizure. This has been a constant phenomenon since the 
beginning of her illness. Occasionally slighter movements of a similar 
kind are seen in the right hand. These movements seem to affect the 
left hand and wrist, but not the elbow or the shoulder. There is no 
wasting. The grasp of the left hand is weaker than that of the right, 
but both cure very feeble. Her sensation has not apparently altered. 
Her knee*jerks are brisk, the left being greater than the right. No ankle 
clonus. The wrist tap is also brisk and the left larger than the right. 
There is very marked increase in the jaw jerk. Plantar reflexes good 
and equal. Her pupils are unequal, the left being larger than the right. 
Both react to light, but the left very sluggishly. There is no ocular 
paralysis or nystagmus. There is very marked tremor of the lower part 
of the face, and especially of the lower lip and jaw. There is also marked 
tremor of the tongue. Her vision and hearing are both good. There is 
no keratitis, Her control over her sphincters is good, and she has only 
once wetted the bed. She has a heavy demented look. Expression accom¬ 
panied by overaction of the muscles of the face. She obeys well. She 
takes no interest in things in the ward, but is like a great child. Her 
speech is coherent but like that of a child, in short sentences. She talks 
but little except in answer to questions or the needs of the time, c.#., 
food, etc., and pain. 

She is careless in her dress and her hair is untidy. She is not 
destructive. No masturbation has been observed. She sleeps well and 
says she does not dream. She has no hallucinations. She is, as a rule, 
decidedly happy and exalted. There are absolutely no delusions of 
grandeur, but she is ahvays quietly happy except w r hen the pain is on. 
She then cries. She sits and smiles all day in stupid happiness and does 
not shout, scream, or sing. She is never melancholy, and only cries 
when the pain in her left side is bad. Her memory is extremely defec¬ 
tive. She says she has been here three weeks ( ~ four weeks) “ as far 
as I can recollect.” She knows to-day is Friday and the month July, 
but does not know the day of the month. She cannot tell in what year 
or month or day of the month her birthday was, but knows she is “ 18.” 



She knows she went to Thames Street Board School. Her multiplica¬ 
tion is very poor. She gets the low r er numbers correctly but hesitates 
greatly over the higher ones. There is no specific loss of memory, but a 
general failure. She is able to visualise well the dresses and caps of the 
nurses and sisters and the quilts. No loss of orientation, w T hich is 
excellent. No delusions. When attacked with the pain in the left hand 
and leg there was a marked rise of temperature. She complains a good 
deal of frontal headache. Her gait is very broad and unsteady, but she 
does not fall with her eyes shut. Romberg’s sign does not give positive 
results. Her grasps are very feeble. There is still no wasting. The 
left pupil is 6 mm. and the right 5 mm. The left does not react to light 
and reacts very sluggishly to accommodation. No oscillation. The right 
pupil reacts well both to light and to accommodation. There is no ocular 
paralysis. There is marked tremor of the face and her tongue is 
extremely tremulous. R.V. L.V. Ophthalmoscopic examination 
of the left eye showed profound grey white stippled atrophy, and the 
right was a dirty pinkish yellow with well marked myopic crescent. She 
is extremely demented and her memory for recent events is gone. She 
cannot tell who has been to see her on visiting day, yet she knows what 
is going on around. 

On October 21, 1897, patient was transferred to Clayburv Asylum 
under the following medical certificate :—Patient is evidently of weak 
mind and her general condition indicates general paralysis in an early 
stage. She laughs in a silly manner without any cause, does not know 
the time of year or day of week. She says that she has plenty of 
money, and when asked how* much she says sevenpence. 

The patient looks as if she had put on flesh. Recognised Dr. Head 
and knew that she had seen him at the hospital. Marked bien etre ; 
marked tremor in the face, muscles and tongue ; ordinary speech fairly 
good, but she cannot utter such test words correctly as “preliminary.” 
She is very tottering in her gait, and in WTiting she has great diffi¬ 
culty in holding and directing the pen, but shows unusual pertinacity to 
write her name. She shows no linear cicatrisation at the angles of the 
mouth, perhaps a slight one at the right angle. The central incisors of 
the upper jaw are somewhat pegged-shaped, notched at the edge, aud 
there is slight linear erosion of the enamel. The pupils are unequal, the 
left larger than the right; react sluggishly to light and accommodation. 
There is marked tremor in the hands, especially on attempting to do any¬ 
thing. Knee-jerks exaggerated, especially the right. Responds to the 
calls of nature. Has had no faints or fits. Is quiet and obedient, but 
shows a progressive dementia. Ophthalmoscopic examination was made 
with great difficulty; grey atrophy.—F. W. Mott. (Vide photo. 4, plate iii.) 

Arterial pressure, 140. Temperature normal. Pressure is very weak ; 
the artery was hardly felt at the w r rist. Heart sounds normal; second 
sound accentuated. She answers questions, but at the slightest sugges¬ 
tion she will burst out laughing. She is unable to recognise colours 
correctly, the only one she knew was red. When writing her name it 
was noticed that she was incapable of any sustained effort; having 
written her Christian name she was quite unable to write her surname. 

PLATE 111 


The inco-ordination becoming more marked as she proceeded, till finally 
she had difficulty in keeping her hand on the paper.—F. W. M. 

October 20, 1898.—Patient is obviously more demented. Her writing 
is much worse; she is incapable of any sustained effort, although she 
tries her hardest, the inco-ordination becoming more marked. She cannot 
hold the pen in the usual way, owing, probably, to her defective tactile 
sense. She holds it between the second phalanges of the middle and 
index fingers with her thumb pressed on the index finger. The nurse 
says that she is more unsteady on her legs. She has a very spastifc gait. 
There are continuous choreiform movements in her right arm, also in the 
left to a less degree. The knee-jerks are markedly exaggerated, triceps 
contraction and wrist tap contraction easily obtained. The nurse says 
she has not had any seizures. Pulse very small, hardly to be felt at 
wrist, arterial pressure 140. Maximum oscillation very limited, only 
about half a degree. 

April 80, 1899. In the same condition, but more paretic and 
demented.—F. W. M. 

Case 11. 

F. B., aged 19, admitted into Claybury Asylum, October 31,1895. 

She was sent from Fulham Workhouse, from which the following 
medical certificate came:—Patient has a silly expression, she has no 
notion of time and says she has been here three weeks. She was 




admitted yesterday. She has the delusion that she is the mother of a 
child in the ward. 

Family history. —No insanity in the family, father, and probably 
brother, died of phthisis. Very little history could be obtained as father 
and mother were both dead. She has a brother a soldier and a married 

Previous history. —Always delicate, did not walk until Bhe was four 
years old. She has never been bright, and has always been backward at 
school, attributed to a fright the mother had when she was pregnant. 
Her present mental condition has evidently been of some duration, for 
she was considered to be dull and silly from childhood. 

Condition on admission. —Height 4ft. 6in. Weight 7st. She has 
three small scars on the neck, said to have been due to an operation for 
swollen glands. Tongue clean. Palate wide and shallow. Teeth 
notched. Congenital sj^philitic. Heart and lungs normal. Pupils 
unequal, left larger than right, sluggish reaction. Muscular strength fair, 
knee-jerks exaggerated. Walk and gait fairly good. 

Mental condition. —Patient is dull, heavy, and cannot answer ques¬ 
tions intelligently. She says she has been here two years (but only came 
yesterday). She can give very little account of herself and is very easily 
confused. Her speech was not affected. Attention poor and memory 
bad. She was considered to be suffering from imbecility.—A. H. Boyle. 

November 5, 1895.—She is suffering from imbecility. She has no 
knowledge or capacity for adding simple numbers. Looks vacant ’and 
listless and says “ ay ” to questions, and that she was all right. Dull, 
stupid and somewhat depressed. Generally below par in comprehension. 
Good general health and condition.—R. Jones. 

November 7.—No improvement, dull and stupid, eats and sleeps well. 

February 7, 1896.—Is in laundry; has been brighter lately, and has 
written a letter. Is very childish and stupid. 

May 3.—Excitable, loss of emotional control. Very childish, works in 

August 27.—Rather brighter and works well as a rule. Dirty habits. 

September 29.—She is an imbecile, says “yes’* and “no” indis¬ 
criminately to questions, or gives quite an irrelevant reply. She is 
childish and laughs in a silly manner for no cause. Well nourished and 
in fairly good health. 

October 20.—Much the same, answers “ yes ” and u no ” to questions. 
Is emotional; is rather troublesome with her food. Had an epileptic 
seizure a week ago. Right arm and leg parescd. Is very constipated. 

February 21, 1897.—Became much worse and stuporose. Wet and 
dirty, having to be fed and made to do everything. Has been in acute 
ward some time. 

March 24.—Came under the care of Dr. Stansfield. Deep reflexes 
exaggerated. Happy and smiling, speech slurred. General tremor. She 
has notched teeth and depressed bridge of nose pointing to congenital 
syphilis. Her symptoms and behaviour, including grinding of teeth, are 
those of general paralysis. 

May 18.—Progressive enfeeblement. She is confined to bed, as she 


falls about and bruises herself. She is very nasty tempered and most 
destructive. Resists any attention paid to her. 

June 20.—In a very low state, constantly grinding her teeth. On 
special diet. 

July 2.—Gradually became worse, and died at 8.55 a.m. 

Post-mortem notes (by Dr. Stansfield).— Post mortem thirty-five hours 
after death. Body emaciated ; post-mortem rigidity present throughout. 
Abrasion of skin over sacrum. Skull —Symmetrical, fair thickness. Dura 
tnater —Thickened, esp^ially so in the inferior parietal and temporal 
regions. Great excess of fluid in subdural space. Pia arachnoid — 
Opaque, thickened, slightly adherent to cortex, adherent to small mass 
in cortex on right side, adhesion between the frontal lobes. Sub-arach¬ 
noid space —Excess of fluid, opaque, gelatinous appearance. Brain — 
Wasted, excess of fluid, pale, 1,040 grms.; convolutions asymmetrical, 
wasted; sulci shallow; cortex firm, pale, small in amount. Small, 
opaque, very hard mass in middle of ascending parietal convolution, size 
of a large pin’s head, replacing cortex. White matter firm. Ventricles 
much dilated, great excess of pale, slightly gelatinous and slightly milky 
fluid. Ependyma slightly granular. Cerebellum, 180 grms.; firm, pale. 
Pons and medulla pale and firm. Spinal cord —Firm. Right pleura — 
Old adhesions, fibrous over whole surface. Left pleura —Old adhesions, 
fibrous over whole surface. Bronchi —Congested; bronchial glands 
enlarged, caseous, and pigmented. Right lung —Several gangrenous 
patches in upper lobe, containing foul-smelling, gummy material, of a 
dark slate colour. Tubercular nodules scattered through whole of lung. 
Weight, 492 grms. Left lung —Discrete tubercular nodules scattered 
through whole of lung. Weight, 884 grms. Heart —180 grms; valves 
normal. Muscular tissue brown in colour, small in amount, fatty, 
fibrous, brown pigmentation. Peritoneum —Devoid of fat. Liver , 875 
grms.; stellate scar on anterior surface; cirrhotic and fatty. Spleen — 
105 grms., firm, congested; small, caseating mass, size of large pea. 
Right kidney —90 graiB; upper and posterior half occupied by caseating 
masses, some becoming confluent. Left kidney —89 grms.; tubercular 
cavity at apex, size of small marble; otherwise no obvious microscopic 
change. Glands large and caseous. 

Cause of death. —General paralysis of insane ; gangrene of lung and 
general tuberculosis. 

Microscopical Examination Notes. 

Examination of the paracentral lobule by Nissl method 
showed thickening of the pia arachnoid, but not much 
inflammatory tissue, nor were the sheaths of the vessels 
much affected in the substance of the brain. The most 
obvious change was in the cells, which were in all stages 
of degeneration, from complete destruction of the perikaryon, 



leaving only the nucleus with the deeply-stained nucleolus, 
to simple chromolytic changes of the cell. Not a single 
cell, however, exhibited the normal pyknomorpbic condition. 
The greater number of them had their processes broken off 
and stained a diffuse dull pink or purple colour. Under a 
high power the cells are seen to be dotted over with a fine 
pink or purple dust; in many instances there is a mere 
shadow of the cell left. The nucleolus alone retains a 
bluish tinge. 

Examination of the cortex and cord by the Marchi Pal 
and Marchi methods:—Tangential system of fibres are 
absent over the ascending frontal and parietal convolutions. 
Stained with carminate of soda, the whole of the superficial 
layers of the cortex are seen crowded with spider cells. By 
the Marchi method sections of the ascending frontal show 
a large number of recent degenerated fibres, and leucocytes 
swollen up and distended with particles of blackly-stained 
fat which are seen lying round the vessels, especially the 
superficial vessels of the pia arachnoid. The spinal cord 
shows scattered degenerated fibres in the lateral columns, 
and especially in the posterior column, but there is no 
sclerosis in the cord. The anterior horn cells show an ex¬ 
cess of fatty pigment stained black with osmic acid. The 
pia arachnoid of the spinal cord is considerably thickened. 
There is no overgrowth of neuroglia cells around the central 

Heart .—Stained by Marchi method, shows recent acute 
fatty degeneration. The striped muscle of the diaphragm 
shows no such change, only indistinctness of striation. 

Liver .—Shows considerable thickening of the capsule 
and overgrowth of fibrous tissue around the vessels, both 
of the portal canal and of the hepatic veins. This fibrous 
overgrowth can be traced in and around the cells, which are 
fatty and atrophied. There is, therefore, pericellular, peri¬ 
vascular and pericapsular fibrosis. 

While in the press, B. L., Case 2, has died. By the kindness of Dr. Camp¬ 
bell I have been enabled to make an autopsy, with the result that the brain 
presented all the usual signs of general paralysis. 


The literature of the Etiology and Pathology of General 
Paralysis is so fully given by Hirschl, “ Die Aetiologie der 
Progressive Paralyse,” that the reader is referred to this 
classical work for a complete Bibliography. Reference can, 
however, be made to the following excellent works and 

Mickle, Julius. “ General Paralysis of the Insane.” 

Tuczek. Beitrfige zur Path. Anatomie und zur Pathologic dcr Dementia 
Paralytica , 1884. 

v. Krafft-Ebing. Die progressive Allgemeine Paralyse. Specielle Path. von 
Nothnagel , bd. ix., 2 theil. 

Mendel. Die progressive Paralyse: Eine Monographic , Berlin, Hirschwald, 
1880, and several other important contributions. 

Fournier. Les affections parasyphilitiques , Paris, 1894. 

Flechsig. Qehim und Seele , 1896, 

Bevan Lewis. “ Text Book of Mental Diseases.” 

Binswanger. Die pathologische Histologic der gross hirnrindenerkrankung , 
bei der Allgem. prog. Paralyse , dc . Jena, Fischer, 1898. 

Binswanger. Zur histologischen Pathol. der Dementia Paralytica Sitzungs- 
bericht der Jenaischen Qesellschaft fur Medicin und Naturwissenschaften , 
June, 1884. 

Esmarck und Jessen. Zeitschrift f. Psychiatric , 14, p. 20. 

Kjellberg. Virchow's Jahresberichte , 1868, ii., p. 10. 

Savage and Goodall. “ General Paralysis of the Insane,” vol. vii. “ System 
of Medicine,” Allbutt. 

Footnote. —I have given a complete Bibliography of the Early Form 
of General Paralysis; but space will not allow me to give a more extensive 
list of references to General Paralysis as affecting the adult. 


Juvenile General Paralysis . 

(1) Alzheimer. “Die Paralyse progressive der Entwicklungsjahre.” 

Neurolog. Centr ., Oct. 15, 1894.—“Die Fruhform der progressive 
Paralyse. Allgem . Zeitsch. f. Psychiat ., lii, f. 8, 1895. 

(2) Bjeljakow. “ Pachyc^phalie et demence paralytique precoce dans un 

cas de syphilis h£r£ditaire.” Wjestnic psychiatrii i neuropathologii , 
vii., 2,1890. 

(3) Bourne viLLE. “Contribution & l^tude de la d&nence 6pileptique.” 

Archives de Neurologic , 1880. Comptcs rendus du service aes idiots de 

(3a) Breslbr. “Einfall von Infan tiler Progressiver Paralyse.” Neurol. 
Centralbl. , 1895, t. 14, p. 1114. 

(4) Bristowe. “ A case of General Paralysis of the Insane at the time of 

Puberty.” Brit. Med. Journ ., Nov. 13, 1893. 

(5) Bury. “ Hereditary Syphilis in the production of Idiocy or Dementia.” 

Brain , Journal of Neurology , 1883. 

(6) Carrier. Note lue au CongrH des Ah&nistes et Neurologistcs de lanque 

frangaise , Toulouse, 1897. 

(7) Charcot et Dutil. “ Sur un cas de paralysie generate debut precoce.” 

Mercredi medical, 1892, No. 6. 



(8) Clouston. “ A case of General Paralysis at the age of 16. ” Journal of 

Mental Science , October, 1877, p. 419.—“The Neuroses of Develop¬ 
ment/* 1891. 

(9) Davidoff. “ Paral. progr. dans le jeune age. ” Russ, archiv. f. Pysch , 

bd. 9, H. 1, 1888. 

(10) Dengleb. These de Nancy , 1893. 

(11) Dunn. “ Case of General Paralysis occurring in a girl,” &c. Journal of 

Mental Science , July, 1895. 

(12) Fournier. Les affections parasyphilitiqucs , 1894, p. 353. 

(13) Elkins, Frank Ashby. The Lancet, 1894. 

(14) Gudden. “ Zur Aetiologie und Symptomatology der Progressiven 

Paralyse, Ac/’ Archiv f. Pscyhiatrie , 1894, t. 26, p. 460. 

(15) Haushalteb. “ Trois cas de paralysie g6n6rale progressive chez 

l*enfant.” SociPtt de dermatologic et de syphiligraphie , Juillet 8, 1897. 
—Annales de dermatologic et syphiligraphie , 1897, p. 761-769. 

(16) Henri. “ Contrib. t\ l’^tude des rapports de la syphilis et de la paralysie 

g6n6rale. (Paralysie gen^rale juvenile paralysie g4n4rale conjugale.)” 
Thpse Bordeaux , 1894. 

(17) Hirschl. “ Beitrage zur Kentniss der progressiven Paralyse im jugend- 

lichen Alter und in Senium.” Wiener Klin. Rundschau , 1885, p. 481. 
—“Die Aetiologie der progressiven Paralyse.” Jahrb.f . Psych., 1896, 
bd. xiv., p. 446. 

(18) Hoch. “ General Paralysis in two sisters, commencing at the age,” Ac. 

Proc . Am. Med.-Psychol . Ass., Utica, 1896; p. 303-318. 

(19) Homen. “ Eine Eigenthumliche bei drei Geshwistern,” Ac. Archiv f. 

Psych., 1891, H. 2, p. 191. 

(20) Huflbr. “Progressive Paralyse bei einem 21 jahrigen Madcheu,” Ac. 

Deutsch. Zeitsch. f. Nerven-Heilkunde, t. ii., p. 478. 

(21) Hughlings-Jackson. Journal of Mental Science , 1877. 

(22) Infeld. Verein fur Psychiatric und Neurolog. in Wien , 1895. — Wiener 

Klin. Wochenschrift , 1895, No. 47. 

(23) Joffroy. CongrPs de mtd. ment ., Blois, 1892, p. 240 .—Mereredi medical, 


(24) Karplus. Verein fur Psychiatric und Neurolog. in Wien , 1895 .—Wiener 

Klin. Wochenschrift , 1895, No. 47. 

(25) Kbafft-Ebing. “Die progressive allgemeine Paralyse.” NothnageVs 

Pathologie und Therapie , Vien, 1894 .—Die progressive allgemeine 
Paralyse , Wien, 1894. — “ Ueber die Zunahme der progressiven 
Paralysis im Hinblick auf die Sociologischen Factoren.” Jahrb. f. 
Psychiatr ., vol. xiii, 1895. 

(26) Legrain. “ Paralysie g6n£rale chez ^adolescent.” Annales de la poly - 

clinique de Paris , 1893. 

(27) Liedesdorf-Salgo. “Uber psychische Storungen im Kindesalter.” 

Wiener Med. Wochensch ., 1883. 

(28) Luhbmann. “ Progressive Paralyse im jugendlichen alter,” Ac. Neuro¬ 

log. Centralbl., 1895, t. 14, p. 632. 

(29) Luys. TraiU clinique et pratique des maladies mentales, 1881. 

(30) Major. “General Paralysis in a boy/* British Medical Journal , 

Dec. 17, 1892. 

(31) Mickle. “ General Paralysis of the Insane.” 2nd ed., London, 1886, 

p. 249. 

(32) Midolemass. “ Developmental General Paralysis.” Journal of Mental 

Science, 1894. 

(33) Mendel. Archio fur Psychiatric, 1865. 

(34) Moussocs. “ De la forme infantile de la paralysie gen^rale.” CongrPs de 

Rome, 1894. Traits des maladies de l’enfance, 1897. Tome iv. 


(35) Nolan. “ Syphilitic General Paralysis.” Journal of Mental Science , 

April, 1883. 

(36) Regis. “Note sur la paralysie g£n6rale pr4matur6e.” L'Enctphale, 

1883.—“ Un cas de paralysie g6n£rale & l’ige de 17 ans.” L'Enc&phale, 
1885.—“ Syphilis et paralysie g6n4 rale.” Archiv. cliniques de Bordeaux, 
1892, p. 287.— Bull . de la soc. de mtd. de Bordeaux, stance du fevr. 23, 
1883.— Ibid., mai 8,1885.— Ibid., d£cemhre 5,1894.— Ibid., 1895.—“ Dis¬ 
cussion & la suite du rapport de Arriaud.” Congr. franc, des mid. alii - 
nistes et neurolog., 8th session, Toulouse, 2 et 7 aodt, 1897. 

(37) Ret et Mani&re. “ Cas de paralysie g£n6rale h6r6ditaire.” Annales 

Mtdico-psychologiques, 1883. 

(38) Saiki. “ Symptomenbild Dementia paralytica im Pubertats-Alter.” 

Berliner Gesselschaft f. Psychiatrie und Nervenkrank. Sitz v., 21 Mai. 

(39) Saint-Maubice. “De la paralysie g6n6rale juvenile.” These Paris, 


(40) Salgo-Weiss. Compend. der Psych. Wien, 1889. 

(41) Savage. “ General Paralysis of the Insane simulating Cerebral Tumour. ” 

Journal of Mental Science, July, 1888. 

(42) Schule. Traiti clinique des maladies mentales. 

(43) Shuttleworth. “Idiocy and Imbecility due to Inherited Syphilis.” 

American Journal of Insanity, Jan., 1888. 

(44) Smith. “ Case of Adolescent General Paralysis of the Insane.” Austral 

M. J., Melbourne, 1895, No. 5, xvii., 497. 

(45) Sommer. “Zum Zusammenhang zwischen Paralyse und Syphilis.” 

Neurolog. Centralbl ., 1886, p. 559. 

(46) Stewart, Purvis. “Three cases of Juvenile General Paralysis.” Brain , 


(47) Stbeitbergeb. “ Ueber die Progressive Paralyse im Jugendlichen Alter.” 

Inaug. Diss ., Jena, 1894. 

(48) Stbumpell. “Einige Bermerkungen uber die Zusammenhang,” &c. 

Neurolog. Centralbl., 1886, p. 434.—“ Progressive Paralyse mit Tabes 
bei einem 13 jaehrigen Madchen.” Neurolog. Centralbl., 1888, No. 5. 

(49) Thiry. De la paralyse ginirale progressive dans lejeune age. 

(50) Thomson and Dawson. “ Case of General Paralysis of the Insane in a 

child.” Lancet, 1895. 

(51) Toulouse. “La paralysie g£n6rale juvenile.” Qaz. des hdpitaux, 24 

aoftt, 1896. 

(52) Turnbull. “Notes of a case of General Paralysis at the age of 12.” 

Journal of Mental Science, Oct., 1881, p. 391. 

(53) Vrain. “ Contribution & l^tude de la paralysie g£n4rale & d£but pre- 

coce.” Thise Paris, 1887. 

(54) Warner. British Medical Journal, April, 1887. 

(55) Westphal. “ Ein fall von Progress. Paralyse bei einem 15 jahrigen 

Madchen.” Chariti annalen, Jahrgang 18,1893. 

(56) Wiglesworth. “ A case of General Paralysis in a young woman, com¬ 

mencing at the age of 15.” Journal of Mental Science , 1883, p. 241. 
—“ General Paralysis occurring about the age of puberty.” Journal of 
Mental Science, 1893. 

(57) Zappebt. “Uber Ursachen von Nervenkrankheiten im Kindes&lter .” 

Wiener Medisinische Wochenschrift, 1897, p. 959. 



A. S., aged 40, admitted to Claybury Asylum October 6, 1896. The 
following are the principal facts which were obtained from the case-book 
relating to this patient’s illness. On admission he was in fairly good 
bodily health ; there is no note relating to venereal disease or alcoholism. 
The exciting cause of the disease is attributed to poverty. His mental 
condition showed grandiose delirium. The knee-jerks were exaggerated, 
the pupils were irregular, and there were marked tremor and slurring of 
speech. He was certified as a case of general paralysis. From this 
time forth to December 16, 1898, the notes throw no fresh light on the 
case, merely referring to the fact that he was becoming steadily worse. 

Abstract of post-mortem notes .—Body emaciated. On the surface 
of the body is a bullous cutaneous eruption. The bull© have in many 
instances undergone sloughing, leaving open sores like acute decubitus. 
They vary in size considerably, and are more or less symmetrical. They 
are not only situated in parts subjected to pressure, such as over the 
heels, the buttocks, the great trochanters, and the elbows, but also on 
the front of the body in situations as indicated in the diagram. By 
inquiry it was ascertained that’these bull© appeared quite spontaneously 
about a week before death. The attendant said that they came like 
blisters. One is indicated in the diagram in front of the right leg. They 
became blue and either dried up, leaving a dark eschar, or if the skin 
were abraded they underwent sloughing, developing where there was 
pressure into deep bed-sores. There was a certain degree of symmetry 
in this eruption, as the diagram shows. The brain exhibited the usual 
naked-eye characteristics of general paralysis. The cerebral arteries 
showed nodular atheroma, and the aorta was atheromatous. 

The spinal cord and spinal ganglia were preserved for microscopical 
examination. Small twigs of the cutaneous branches of the anterior 
crural nerve going to the bull© indicated by two lines in fig. 1 were care¬ 
fully dissected out, and portions of the same cut off prior to their 
entrance to the bull©. Placed in Marchi fluid and left for twenty-four 
hours, washed thoroughly with distilled water, and then dissociated with 
needles and mounted in Farrant’s solution, about one in five fibres 
were found to be degenerated. See fig. 2. 


Fig. 1. 

The patches shown on the body were the seat of bull® which appeared 
spontaneously in various situations, and rapidly developed into eschars. The 
above drawing to indicate their situation was made on the post-mortem 
table. They are not recorded in the notes. 

Fig. 2. 

Teased preparation of a nerve twig of right anterior crural going to bulla 
on right leg. Magnification 300. 



Spinal Cord. 

Cervical region .—The anterior third of the posterior median columns, 
except where they abut upon the posterior commissure, is markedly 
sclerosed. From this point a band of sclerosis passes outwards and 
backwards into the bases of the postero-extemal columns, not, however, 
reaching to the periphery’ of the cord. It is separated from the mesial 
margins of the dorsal horns by a moderately 'thick fringe of fibres and 
from the posterior two-thirds of the postero-median columns by the 
intermediate septum. The posterior two-thirds of the postero-median 
columns are the seat of a slight diffuse sclerosis. Charcot’s root zones 
are normal. There does not appear to be any fibre atrophy or sclerosis 
of Lissauer’s tracts. External to the cord the cervical afferent roots are 
almost healthy. Occasionally a wasted fibre can be seen. The fibres 
of the cornu-commissural zone are intact. In the position of the crossed 
pyramidal tracts is a slight diffuse sclerosis. By Marchi’s method about 
a hundred degenerated fibres may be counted in the left tract, in the 
right about three times as many, and fifty or sixty in the opposite direct 
motor tract. In the right direct tract a few only can be seen. The 
antero-lateral descending tracts on both sides contain degenerated fibres, 
about 160 on the left, and half as many on the right side. The grey 
matter appears to be sound. 

Thoracic region .—The posterior tw'O-thirds of the posterior-median 
columns are slightly and diffusely sclerosed. There is a slight atrophy of 
fibres in the root zones. The postero-extemal columns in their median 
aspects are markedly sclerosed and almost denuded of fibres. The 
anterior part of the sclerosed patches slightly encroach upon the position 
of the comma tracts and pass backwards into the root zones. External 
to the cord many root fibres have entirely disappeared. The right 
pyramidal tract is apparently more markedly sclerosed than in the 
cervical region. On the left side sclerosis is slight. A few fibres are 
atrophied in the left direct motor tract. 

Lumbosacral region .—There is a moderate degree of fibre de¬ 
generation and sclerosis in the posterior columns. About one-third of 
the fibres have almost disappeared. Many existing fibres are in various 
stages of atrophy. Charcot’s root zones are partially sclerosed, as are 
also Lissauer’s zones. The posterior roots contain a number of degen¬ 
erated fibres, but are not much sclerosed. There does not appear to be 
enough fibre atrophy in the roots to account for the sclerosis in the 
columns. The median triangle and the fibres that lie betw een it and the 
periphery of the cord are intact; and also those that are in the position 
of the cornu-commissural zone. The right crossed motor bundle shows 
a greater degree of fibre atrophy and sclerosis, than in any higher level. 
The same is true of the left fasciculus. This is no doubt due to the fact 
that the leg fibres were the most affected. But here, as in the higher 
planes of the cord, the latter is only slightly implicated compared to 
the former. In the position of the left descending antero-lateral tract 
are a few degenerated fibres. With the exception of a slight rarefaction 
of that part of the dorsal horns through w’hich coursed the atrophied 

Plate IV. 

' .■ . jm' V 




Fig. 1. 

Cortical pyramidal cells from a case of typhoid with continued high fever. 

Magnification BOO. 

✓ * 

•/ T&4 

* * 

k J, 

mm. ;?■ 

r ' * -Mnjygy., ■- g T > < X 

*s. v v 

* j , ■«•-.. . cu^ ~ -.4 i? 

? «bL« r * ■ p 'iiT' K 

*»p' X 

Fig. 2. 

Drawing illustrating appearances of cells of fourth lumbar spinal ganglion, right 
side, from case of general paralysis with bullous eruption. 

Magnification 300 diameters. 

J. W. B.j dtl . John Bale, Son j <£ Danul&ori, Ud. t tendon, W. 

1 0 JdGt p. Jvv. 


posterior root fibres, the grey matter is healthy. In no plane dp the 
anterior roots contain unsound fibres. In the next number of the 
Archives these cord lesions will be figured in conjunction with a number 
of other tabetic cord lesions occurring in general paralysis. 

Posterior root ganglia .—The first lumbar ganglia contain a few de¬ 
generating cells. The chromophyllic granules in such cells are distributed 
through the body as a pale fine dust. Along the margins of a few is a 
band of clear homogeneous plasms in which no chromophyllic granules 
can be seen. Occasionally a segment of this clear band is seen breaking 
down. The nuclei are normal in position but extremely pale. The 
nucleolus is unaffected in most instances. In the third, fourth and fifth 
lumbar ganglia the number of degenerating cells is larger; quite a quarter 
of the cells in each section present an extreme atrophy. The nucleus 
has lost its membrane, and is now' a pale rough margined disc lying in 
the wholly unstained homogeneous body plasm. Here and there a cell is 
to be seen with rough granular edges as though about to disintegrate. 
Many other cells are in a less advanced stage of atrophy. Nucleus and 
nucleolus are apparently normal. But the body plasm is thickly strewn 
with exceedingly fine broken-down chromophyllic granules. In one part 
of the cell body this chromophyllic dust may be very pale and almost 
homogeneous, as though the cell was approaching the above described, 
probably more advanced stage of atrophy. Spaces containing no cells 
are numerous. In some of these is a fine coarsely granular unstained 
debris, the remains of wholly degenerated cells {vide plate iv., fig. 2). 
The distal and proximal fibres of all the lumbar ganglia are apparently 
normal in the sections examined. It is conceivable that the changes in 
the ganglion cells are secondary to the degeneration of the nerve-fibres. 



ENG. ; M.R.C.P.LOND., 

Late Technical Research Scholar. 

This research has been undertaken, at the suggestion of 
Dr. Mott, with the object of ascertaining if any changes are 
recognisable in the pneumogastric and the sympathetic 
nerves in advanced general paralysis of the insane. Ten 
cases have been examined, and the sections made contrasted 
with other sections obtained from cadavera of patients not 
affected with general paralysis. The vagus has been studied 
between the jugular canal above and the level of the roots 
of the lungs below, by means of numerous transverse and 
longitudinal sections. The sympathetic nerves examined 
have been the cardiac branches of the vagus and the nerves 
around the coronary and splenic arteries. The cadavera 
were, in accordance with custom, placed as soon as possible 
after death in a chamber kept at 0° C., where they remained 
until the autopsy was made, generally six to twenty hours 
after death. 

Anatomical data. 

Before proceeding to describe the condition of the vagus 
elements it is necessary to refer in some detail to the method 
of examination of this nerve which was adopted, and to 
enumerate several points in the normal structure and dis¬ 
position of the vagus which bear upon the enquiry. In the 
first instance sections were made transversely at the levels 
A to F, figs. 1 and 2, the various branches being also cut 
separately in some cases, in order to check the conclusions 
arrived at as to the composition of the main trunk. Longi- 


ftgl- Fig.H 

Fig 1. 

Transverse sections of the right vagus nerve in the adult at the different 
levels indicated in the next figure. Most of the larger branches which can 
be identified are shown in the sections. Sup . lar. n., superior laryngeal 
nerve; r. 1. n., recurrent laryngeal nerve; inf. c. c. n., inferior cervical 
cardiac nerve; c. brs. t cardiac branches. A, section above the inferior 
ganglion of the vagus (including also the hypo-glossal nerve); B, section 
through the middle of the inferior ganglion; C, at origin of superior 
laryngeal; D, at origin of the inferior cervical cardiac nerve; E, through 
recurrent larvngeal nerve close to its origin : F t through main trunk of vagus 
close below the origin of the recurrent laryngeal nerve, x 9. 

Fig. 2. 

Diagram of the right vagus nerve in the adult showing the various levels, 
A to F , at which the transverse sections represented in the preceding figure 
were made. Gl.-ph. n., glosso-pharyngeal nerve; s. a. «., spinal accessory 
nerve; phar. n., pharyngeal nerve ; i. g. 9 inferior ganglion of tne vagus. The 
remaining letters are the same as in the preceding figure. This diagram is 
slightly less than the actual size. 



tudinal sections were also made at and between the levels 
indicated. The cases examined in this way do not, owing 
to variations in the arrangement of the nerve-bundles, 
enable a general diagram of the structure of the vagus at 
different levels to be given; figs. 1 and 2 represent an 
individual case. The superior ganglion of the vagus owing 
to the density of the fibrous structures surrounding it cannot 
easily be examined, and is liable to injury during removal. 
The inferior ganglion is, however, readily isolated. The size 
of the sectional area of the nerve is influenced by several 
circumstances, particularly the degree of stretching or re¬ 
laxation present during the hardening process, and the amount 
of connective tissue in the sheath of the nerve. Very thin 
sections are apt to become altered in size during the process 
of cutting; in contrasting the sectional appearance of the 
nerve at different levels it is therefore necessary to select 
rather thick sections ( i.e ., about 20/a in thickness). 

The appearance of transverse sections of the vagus at 
and above the level of the inferior ganglion (B and C, fig. 1) 
varies in different cases rather widely, owing to the large 
number of separate filaments which in this situation undergo 
a partial coalescence, and immediately afterwards present a 
rearrangement in view of their peripheral distribution. The 
arrangement of the nerve-cells in the inferior ganglion is 
not the same in all cases. Sometimes the groups of nerve 
cells are gathered to one side of the main trunk, and a certain 
number of nerve fibres do not appear to be in relation with 
the nerve-cells. Not unfrequently, as in fig. 1 B, numerous 
nerve-bundles are seen separated from the main trunk, 
which contains the groups of nerve-cells. It is, however, 
not uncommon for nerve-cells to be found here and there in 
the smaller nerve-bundles existing by the side of the ganglion, 
and occasionally nerve-cells are found in the main trunk 
below the ganglion, as well as in the larger bundles above, 
from which the main trunk is derived. It will thus be seen 
that the limits of the inferior ganglion are not very sharply 
defined. The nerve-cells of the inferior ganglion of the 
vagus have a capsule containing numerous nuclei, and closely 
resembling those of the ganglia on the posterior roots of the 


spinal nerves, with which the inferior ganglion is generally 
regarded as homologous. 

At the level of the inferior ganglion some difficulty is 
experienced in identifying the separate nerve bundles and 
in recognising the strands of fibres from the division of 
which they are derived. Some help is given by a com¬ 
parison of the nerve-bundles seen in transverse section 
with sections of the nerve branches and main trunk at 
a slightly lower level, where identification is readily made 
owing to the separation of such of the bundles as proceed 
to their peripheral distribution. Assistance is also afforded 
by the preponderance of large medullated fibres in some 
nerve-bundles, e.g., the superior and inferior laryngeal 
nerves, and their sparseness in others, e.g., the cardiac 
nerves (fig. 4 a). The larger nerve branches often divide 
into numerous small bundles before they leave the main 
trunk, and when these latter are not closely bound together 
in a single sheath, their identification may be difficult. The 
superior laryngeal nerve is generally well defined at the 
level of the lower extremity of the inferior ganglion, and 
can he readily identified by its sectional appearance and the 
large number of medullated fibres it contains. The pharyn¬ 
geal nerve consists sometimes of a single trunk, sometimes 
of numerous small twigs, and contains a large number of 
medullated fibres. In the thorax the cardiac and cardio¬ 
pulmonary nerves are much more readily recognised. Some¬ 
times an inverse proportion appears to exist between the 
size of the cervical and thoracic cardiac nerves. Mot 
unfrequently it is not possible to display the cervical- 
cardiac nerves satisfactorily by means of dissection. 

From the above it is readily understood that by making 
transverse and longitudinal sections in a relatively small 
number of situations, a complete examination of the con¬ 
dition of the main trunk and principal branches of the vagus 
is easily made. 

The examination of the cardiac nerves may, as already 
indicated, conveniently be made together with that of the 
vagus. Owing to the delicacy of these nerves great care 
must be taken not to inflict any mechanical injury upon 
them during removal; all manipulation is to be avoided. 

ddfi akchivch 

■■During hardening, the. vagus with the cardiac and :o'lb«r 

branches was kept very slightly stretched 

The qiitdiac Rejrvhfc arodiid the, bterpuaty .arteries vr'eVe 

'-studied by excising these arteries with the tissues imine- 
■■ . 

tiiately surrounding them, and proceeding to section without 
further dissection! The..• art-eriea fixed 'oh cork wet* 
.tiarthined in Marohi's fluid so as to tJffferentiate the medul- 

The examination of the splenic nerves was similarly made 
by excising the splenic artery with /the nerve-plexus sur¬ 
rounding it intact, fixing orr ct>rk ttud harrletiing in March?* 
Ur! ni 


. : F!<S> 

. Transverse section rtf u portion of tho trunk of the vagus j,i»low the orfgftf 
of the aaporior i«.ryngea) nerve (at level L>. fig, 2). Largo iwetfuflatodj shiftf! 
a'lehUlatcd and oofi-uiedullateil fibres JUft isofi/ th« 

'K»iw.'Odijs nuclei of the primitive sheaths are slso secti. v- iSO ilhjTue 
shiS and safrahiDj fteoeval Paralysis of thiilnUttOe-. 

Method op Examination op 3$ehve-K watt^rs. 

The nerve-fibre* present: in the vagufi'(fig, H) ate divisible 
into three* groups : large, meduilated nerve-fibres,-measuring 
from. 8‘7 f u to I.*2g.; small, medullated ijervts-fihfe.s, haying a 
thinner coating of myelin and measuring to 7 //; and 


non-medullated fibres, measuring 1/z or 2/t to 4i/z. The 
first are numerous in the laryngeal and pharyngeal nerves ; 
the second are conspicuous in the trunk of the vagus (fig. 3); 
and the third predominate in the cardiac, coronary and 
splenic nerve-bundles (fig. 4) which, however, also contain 
a very limited number of small, raedullated nerve-fibres. 

The medullated fibres, large and small, were stained 
with osmic acid, being placed, as already mentioned, imme¬ 
diately after removal in Marchi’s fluid. The axis-cylinders 
were examined by hardening in Muller’s fluid and staining 
by Stroebe’s method. For the examination of the non- 
medullated fibres, osmic acid staining was found to be 
essential, as by it alone can the non-medullated be dis¬ 
tinguished with certainty from the small, medullated fibres. 
By further staining with methylene-blue, using alcohol 
alone or with the addition of 10 per cent, of anilin oil as 
a decolouriser, the primitive sheaths of the non-medullated 
fibres are rendered clearly defined and the nuclei of the 
sheaths are at the same time stained darkly. Safranin 
staining also gives good results. The examination of the 
non-medullated fibres is less readily made than that of the 
medullated nerve-fibres, in consequence of the tendency to 
osmotic changes occurring during the preparation of the 
tissue, causing irregular swelling of the fibres, which thus 
assume a varicose or moniliform aspect. The same appear¬ 
ance may, indeed, be also seen in the smaller medullated 
fibres. It is to a great extent diminished, though not as 
a rule wholly avoided, by removing the nerve with as little 
delay as possible after death and placing it at once in 
Muller’s or Marchi’s fluid. The non-medullated fibres are 
also very easily torn during section-cuttmg or mounting, 
and, again, if the nerve is subjected to compression the 
individual bundles of which it is made up become com¬ 
pressed into almost homogeneous-looking masses. 

In examining the vagal ganglia, after hardening in 
Muller’s or Marchi’s fluid, staining with safranin, hsema- 
toxylin and eosin and methylene blue was practised. The 
condition of the chromoplasm was observed by hardening in 
alcohol and staining by Nissl’s or Held’s method. 




The Condition of the Nerves studied in General 
Paralysis of the Insane. 

As already stated, ten typical cases of general paralysis 
of the insane were selected for examination. In seven of 
these the condition of the vagus was studied : in four the 
condition of the cardiac nerves was noted, and in three the 
condition of the splenic nerves was observed. In individual 
cases also, it may be added, the condition of the phrenic, 
glosso-pharyngeal, spinal accessory, genito-crural and hypo¬ 
glossal was noted, but only a single observation was made 
of each of these nerves. The upper and lower ganglia of the 
vagus were examined in four cases. 

No abnormal appearances have been encountered in the 
large and small medullated nerve-fibres of the vagus and 
its chief branches (c/. fig. 3), though numerous sections, 
longitudinal and transverse, have been carefully examined 
at the various levels of the main trunk already described, 
as well as some of the chief branches. The myelin sheath 
is of even thickness, and stains equably with osmic acid ; 
no degenerated fibres have been encountered in the cases 
examined, with the doubtful exception of a single nerve- 
fibre found in one vagus trunk in the superior mediastinum. 
The axis-cylinders stain well with anilin blue, and the 
basophile material lying between the axis cylinder and the 
primitive sheath does not appear to be increased in amount 
or to stain with unusual intensity. The nuclei of the 
primitive sheath are not increased in number. 

No changes are observable in the connective tissue 
surrounding and supporting the nerve-fibres or in the blood¬ 
vessels of the nerves. The sectional appearance of the 
vagus at different levels presents, as already mentioned, some 
variation in different cases; in the cases of general paralysis 
which have been studied, there has not been found any 
special character differing from the normal. 

The result of the examination of the other mixed nerves 
referred to above has also been entirely negative; no 
degeneration has been found on careful search nor have 
any other morbid changes been observed. 



Similarly the* non - n ted u 11 used nerves, whether studied in 
thofri&in trunk ot the vagus as in fig:-. 8, m in the cardiac 
(fig. 4 #, % eororntry or nerves, have hot 

Flo. i. 

Transverse, a, and longitudinal, 6, sections ai a cardiac nerve . Iran* 

Transverse, tt, and longitudinal, b, sections si a cardiac nerve . transverse 
section of a splenic nerve-bundle, tn a feh* nerve-t.\t’ig isi «cen to be made up 
: chJs#y.of non-mi^aUai^ nacini ot vyhUdi lira ; 

ftidel three small meduUated irbre^ are *ttc>tyo neat lM$ The aou- 

n^dullated fibres show- tenringv tn b $ longitadmal ; «eetion r 

of the same n&r*4 ifi nnij* -lnednjiiatea.:fibre* are bare pr^tik In c 
& micceBsful prejjani.tfda^blf.- A norve ;Iin& Won With the 

exception of two inyetin.^ted fit?rcs v onJy non *tfjcdsjlVuU^ flbres ArH w. 
Numerous nuclei belonging to tiie primitive sbeatbs and a 

portion nt tiie counct tivo fexae of the p* to >. %%5 

Qsmid acid And dv>tUy!ene* -fje‘n<->ral P*,raly>4« cdtb* Inm/n.- 

appeared to be altered ; no cbdngt* lnt& been" noted in the 
primitive sheath* or their nuclei, nor have the conducting 
fibres themselves presented u.u.y recognisable abnormal 
character. The connective tissue smTou tiding' the ' libh- 
medulluted fibres also fajIs to exhibit niiv ishahhe* 



The cells of the lower ganglion of the vagus were in one 
case examined by Nisei’s method. The chromoplasm was 
found to be present in the form of very fine granules, though 
occasionally coarser granules were found in some of the 
largest cells. In some of the cells there appeared to be a 
deficiency in staining reaction, but generally when the cells 
did not stain well the defect of staining was merely apparent 
and not real, being due to the cells being cut in two and 
thus being lighter in tint. Apart from this, however, there 
was in some of the cells a defect in chromoplasm. A few of 
the nuclei were eccentric, a few being quite at the periphery 
of the cell; but none are completely, or even partially, ex¬ 
truded. The nuclei were found to be clear, and the nucleoli, 
generally single, were deeply stained. No vacuolation was 
present in any of the cells, and only a very small number of 
the cells showed commencing pigmentation. 

In several other vagal ganglia, superior and inferior, from 
cases of general paralysis, stained with logwood and eosin, 
no abnormality in the appearance of the nerve-cells could be 
asserted. The capsules of the ganglion cells were multi- 
nucleated. The blood-vessels were sometimes congested, 
but were otherwise unaltered. There was no increase of 
the connective tissue of the ganglia. 


In the vagus and sympathetic nerves studied in general 
paralysis of the insane, the methods of examination 
employed yielded negative results. No evidence of 
degeneration of medullated nerves could be obtained in 
the ten cases investigated (with the exception of a single 
fibre, in which degeneration was found, and which was 
therefore presumably an accidental occurrence). Nor did 
the non-medullated fibres show any abnormal aspect. No 
alteration was found in the connective tissue surrounding 
the nerve-fibres. I am thus able to confirm the opinion 
expressed by Dr. Mott in his 1897 report, viz., that the fatty 
degeneration of the heart and other muscular structures 
which he found in general paralysis could not be accounted 


for by recognisable degenerative changes in the vagus or 
sympathetic nerves. Dr. Mott, I may mention, not only 
employed the various methods which I have adopted, but 
also dissociation after staining in osmic acid the fresh 



At Dr. Mott’s suggestion I have examined the tangential 
fibres in the hind part of the third frontal gyri of the 
following sixteen cases. The possible significance of the 
atrophy has already been referred to by Dr. Mott. 

Method by which Weights were determined. 

The cerebellum pons and bulb are separated from the 
cerebum by a transverse cut through the crura cerebri close 
to the pons. An accurate median section of the brain is 
then made by pressing the median surfaces closely upon 
the knife, and cutting downwards. The ventricles are 
opened, any cerebral spinal fluid they may contain turned 
out, and each hemisphere allowed to drain for a few minutes 
before its weight is taken. It may seem that this method 
is too rough, and full of possibility of error. For first of all 
it is apparently difficult to make a clean and accurate median 
cut. Practice, however, skills one to do this so well that the 
most captious critic would be satisfied. And, again, should 
the knife clip off a piece of one hemisphere, it can easily be 
detected, the clipped-off part removed, and weighed with its 
own hemisphere. 

It may, therefore, be fairly claimed that all gross error is 
eliminated by proceeding as detailed above, and that- the 
weights given represent as near as possible the true difference 
between the halves of the various cerebri. 


Parts Removed and Method of Preparation. 

In every case the posterior thirds of the lowermost frontal 
convolutions were taken for examination. The pia arachnoid 
was not removed, because if this is done it disturbs, in fact 
may destroy, the molecular layer of the cortex. These 
portions of the cortex were divided into halves by an antero¬ 
posterior cut, and one portion placed in absolute alcohol and 
one in Muller’s fluid. The tissue fixed in absolute alcohol 
was prepared for cutting by the paraffin method. Right and 
left blocks of tissue were cut in the same bed of paraffin 
at a uniform thickness of 15 microns. The sections were fixed 
to cover slips, and stained by Nisei’s method. Thus from 
beginning to end of the process of preparation the conditions 
were the same for both right and left sections. The pieces 
fixed in Muller’s fluid were stained by the Schafer-Pal 
method, after the sections had been cut in the same blocks 
of celloidin to a uniform thickness of 25 microns. 

It may be stated at once that there is no sure difference 
in the degree of atrophy in the cells of the two sides as 
shown by Nissl’s method. This part of the research may 
therefore be dismissed from further consideration. 

Clinical History and Pathological Anatomy of the 
Tangential Fibres of the Various Cases. 

In each case the age, sex, duration of symptoms, and only 
so much of the clinical observations as is needed to show 
that it was general paralysis, are given. None of the cases 
were specially picked. They are the first sixteen cases 
that died at Clay bury after December 1, 1898. 

N.B.—The case of Tabetic General Paralysis of which 
a photograph of the two hemispheres is shown in plate i. 
gave very definite results. The tangential fibres had quite 
disappeared on the left side, but were present in considerable 
numbers on the right.—F. W. M. 

Weight in * 

grammes of 

Name. Age. Sex. Duration of Symptoms. Mental Symptoms. Motor Symptoms. hemispheres. Cause 0 f Death. Microscopical Examination. 


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BY F. W. MOTT, M.D., F.R.S., 



Late Technical Research Scholar . 

In nerve degeneration, staining by Marchi’s method 
reveals alterations in the chemical constitution of nervous 
tissue, in the form of change in the composition of the 
myelin sheaths and axis-cylinder processes. Marchi’s 
method consists in first fixing small pieces of tissue in 
Muller’s fluid for at least fourteen days. The pieces of tissue 
are next placed for six to twelve days in a mixture of two 
parts Muller’s fluid and one part of a 1 per cent, solution of 
osmic acid. After thorough washing they are then em¬ 
bedded in celloidin and cut. 

The Appearance of Degeneration. 

The degenerated nerve-fibres when stained by Marchi’s 
method appear in transverse section (fig. 1(f) as round black 
masses occupying the whole thickness of the nerve-fibres 
and contrasting with the ashy grey rings with a clear centre 
formed by the normal myelin sheaths still remaining. In 
longitudinal section (fig. lc) the degenerated fibres appear 
as elongated black masses, broken at intervals and of 
irregular shape, while in some of the fibres in which the 
degeneration is more advanced lines of black globules exist. 
In recent degeneration also the breaking-up of the axis- 
cylinder can sometimes be recognised as in fig. 2, which 
represents a longitudinal section of the spinal cord of the 
monkey six days after hemisection. 

The Duration of Degeneration. 

The degeneration of nerve-fibres when produced experi¬ 
mentally can be recognised at the end of six days (as in fig. 

1 This was communicated to the Physiological Society on Feb. 18, 1899, 
and an abstract of the paper appeared in the Proceedings of the Society, 
Journal of Physiology, vol. xxiv., No. 1. 



2). It persists for long periods; for example, it can be 
recognised at the end of eighteen months, though less 
marked than when examined at earlier periods, but ulti¬ 
mately it is replaced by sclerosis. As the degenerated 
masses begin to disappear it is found that the leucocytes in 
the neighbourhood of the blood-vessels of the tissue con¬ 
tain fatty granules which they have evidently taken up 
from the tissue. 

Degeneration in other Tissues. 

The same type of degeneration is seen in other tissues, 
as in striated muscle and in parenchymatous organs, liver, 
kidney, &c. 

Vegetable tissues, as, for example, Brazil nuts and 
almonds, after hardening with Muller’s fluid, will stain black 
with Marchi’s fluid owing to the presence of neutral fat. 

Nature of Nerve Degeneration. 

"When degeneration takes place in nervous tissue the 
fat which is set free and is revealed by Marchi staining has 
two sources of origin : (1) decomposition of myelin; (2) 
decomposition of protoplasm of the axon. The protagon 
which is a phosphorised fat contained in the myelin, splits 
up into glycero-phosphoric acid, stearic acid and choline, 
and the stearic acid radicles probably unite with the glyceryl 
radicles to form neutral fat according to the generally 
accepted explanation of nerve degeneration. The formula 
for lecithin is 

C - H ‘| o-ro°1' OH 

1 U t O — C,H 4 — N(CH,),OH 

and the equation representing the above-mentioned decom¬ 
position is— 

C„ H„ NPO, + 3H,Q = 2C„ H„ 0, + C, H, PO. + C, H„ NO, 

(lecithin) (water) (stearic acid) (glycero-phosphoric acid) (choline) 

The degeneration of the axis-cylinder (fig. lc), which 
occurs early, is akin to fatty degeneration occurring else¬ 
where, in protoplasm for example, in striated muscle. The 
splitting up of phosphorised fats into simpler compounds 
in cases of degeneration is probably one of hydration, as 



is supported by the experiments of one of us on monkeys’ 
cords, the excess of fat arising from the lecithin which has 
decomposed. Again, one of us, in conjunction with Prof. 
Halliburton, 1 has found that in brain disease when cerebro¬ 
spinal fluid is in excess and rapid wasting of the brain 
substance has taken place, e.g., in general paralysis, the 
cerebro-spinal fluid contains choline. This is an indirect proof 
that the lecithin of myelin breaks up in the way above 
indicated. In a paper published on another page further 
evidence is given of the defect of phosphorus in degeneration 
of nervous tissue, derived from numerous analyses of brains and 
cords in general paralysis of the insane and other conditions. 

In order to study still further the chemical changes 
occurring in degenerated nervous tissue, and as far as 
possible to express these changes quantitatively, the examina¬ 
tion of the spinal cord in cerebral hemiplegia, which forms 
the object of the present research, was undertaken. In the 
spinal cord in hemiplegia of cerebral origin the degeneration 
which occurs is pure, the cord being at some distance from 
the seat of the lesion causing paralysis. 

Previous observations. 

In a preceding observation made by one of us * a spinal 
cord from a case of left hemiplegia was split longitudinally 
into two halves, and the ether extracts of the two sides 
compared. It was found that the right half-cord contained 
10 per cent, of lecithin in the dried ethereal extract, the left 
half 815 per cent., and if allowance was made for the direct- 
pyramidal tract which was well marked, the loss of lecithin 
in the degenerated pyramidal tract would be about 3 per 
cent. There was also more water on the degenerated side, 
as well as more fat, and the extract on the degenerated was 
different from that on the sound side ; the former having 
an appearance like butter, the latter consisting of a crystal¬ 
line substance. It is evident, however, that there was some 
mistake either in the calculation or the mode of examination, 
for the amount of lecithin on the sound side was about half 

1 Proc. Roy . Soc April, 1899. 

2 The General Pathology of nutrition. “ Allbutt’s System of Medicine," 
vol. i., p. 189. 


what it should have been. The two following observations 
were made upon spinal cords taken from two cases of 
cerebral hemiplegia, with the view of more accurately 
investigating the changes in the chemical constitution of 
nervous tissue occurring in degeneration. The results ob¬ 
tained, although differing in the percentage of lecithin, en¬ 
tirely agree in principle with the above-recorded observation. 

History of Cases examined. 

The first case was that of a woman, 55 years of age, 
who had an attack of left hemiplegia fourteen days before 
death. The symptoms of hemiplegia were in every respect 
typical and at the post-mortem pontine haemorrhage was 
found, the blood-clot passing forwards to the right optic 
thalmus. The notes of this case will be published more 
fully in a further communication by Dr. E. Smith. The 
second case was that of a woman 59 years of age, suffering 
from left hemiplegia, which dated back to fourteen days 
before death, and having a history of a hemiplegic attack 
some time previously, involving the opposite side. At the 
post-mortem , the right internal capsule exhibited several 
spots of softening and cysts containing yellow fluid. 

Histological Changes in Cord. 

A section of the first case in the cervical region (fig. 1, 
Case 1) shows by Marchi’s method marked degeneration of 
the left crossed and the right direct pyramidal tracts. 
There is also some slight degeneration of the right crossed 
pyramidal tract, and a few scattered fibres are found de¬ 
generated in other parts of the cord, particularly in the 
right antero-lateral descending cerebellar tract and the left 
direct pyramidal tract. 

A section of the eighth cervical segment of the second 
case stained by Marchi’s method (fig. 1, Case 2) exhibits a 
greater degree of degeneration than the previous section. 
The degeneration is most marked in the left crossed and 
right direct pyramidal tracts. The right crossed pyramidal 
tract exhibits a lesser degree of degeneration and there are 
a few scattered degenerated fibres elsewhere, particularly 
in the right antero-lateral descending cerebellar tracts and 



also in the left antero-lateral ground fibres and adjoining 
portion of the left anterior horn. The large cells in the 
right anterior horns in both sections contain black granules, 
while in the left anterior horns the cells are similar, or more 
frequently are represented by much smaller collections of 
dark granules. When the two sections are compared to¬ 
gether side by side, they are, as in fig. 1, seen to re¬ 
semble each other very closely as regards the distribution 
of the degeneration, and there is little in Case 2 to suggest 
a previous attack of hemiplegia affecting the opposite side. 

The section of Case 2 shows a contraction on the right 
side. By sketching under Edinger’s apparatus to a magni¬ 
fication of about twelve diameters and estimating the weight 
of paper covered by the two halves, it was found that the 
right half of the cord covered 6 per cent, less paper than 
the opposite. 


The spinal cords after removal from the body were 
stripped of dura mater and arachnoid and the nerve-roots 
cut close to their origin. The cords were then divided 
longitudinally, as nearly as possible in an antero-posterior 
mesial plane and the two halves weighed. Unfortunately 
in the first cord some delay occurred before this division was 
effected and a certain degree of desiccation occurred, so 
that in this cord the percentage of water in the halves could 
not be determined. After weighing, the first half-cords 
were dried by sulphuric acid under diminished pressure in a 
desiccator, first at 0" C. and subsequently at 15° C.; the 
halves of the second cord were kept at 60° C. until most of 
the water was driven off, after which drying was completed 
in a desiccator by sulphuric acid under diminished pressure 
at 15° C. As soon as the half-cords possessed the necessary 
degree of stiffness, as drying proceeded they were cut up 
into small fragments with a pair of scissors with a view to 
extraction. After drying, the half-cords were extracted with 
dry ether in a Sohxlet apparatus. At the end of two days 
the flasks were changed and extraction continued for another 
day, when only a few milligrammes more of extract was 
obtained. After extraction was complete, extract and 



residue were again dried, first at 60° C. in an air-oven and 
afterwards in a sulphuric acid desiccator under diminished 
pressure at 15° C., and the combined weights compared w ith 
the original weight of the corresponding half-cord. The 
extracts and residues were then brought into contact with 
fused caustic soda containing nitrate of potassium, when 
the whole of the organic matter was got rid of at a tempera¬ 
ture below redness and the phosphorus present converted 
into sodium orthophosphate. This was precipitated as 
phosphomolybdate of ammonium and subsequently as 
ammonio-magnesium phosphate, which after removal of a 
trace of molybdenum, was weighed as pyrophosphate of 
magnesium. In carrying out this analytical procedure, 
every care must be taken to secure accuracy, especially in 
the later stages, otherwise the errors of experiment are 
likely to exceed the variations in chemical composition of 
the half-cords caused by the pathological process. In the 
ether extract, most of the phosphorus present appears to be 
in combination in the form of a phosphorised fat compound. 
It will be convenient, as affording some idea of the amount 
of phosphorised material present, to calculate the amount 
of lecithin which would be contained in the various extracts 
if the whole of the phosphorus present were in the form of 
combination. This assumption has been made in every 
case, as affording a means, perhaps not very accurate, of 
comparing the half-cord extracts in respect of phosphorised 
and other constituents which would otherwise not be 

Result of Analyses. 

The results of analyses made are given in the accom¬ 
panying table: 

In Case 1 (left hemiplegia of fourteen days’ duration) the 
right half of the cord was made up of 38 9 per cent, of 
extract soluble in ether and 61T per cent, of proteid residue, 
as against 42T per cent, extract and 57 9 per cent, residue 
in the left half of the cord. Assuming the whole of the 
phosphorus contained in the extract to be present in the 
form of lecithin, there would be 22'2 per cent, of lecithin 
and 16'7 per cent, of other extractives in the right half-cord, 



while the left half-cord would contain 18'9 per cent, of the 
former and 23 2 per cent, of the latter. As the right half 
must be taken as approximating to the normal type, and 
the left as typical of degeneration, we see that in degenera¬ 
tion there is a relative increase in the ether extract at the 
expense of the proteid residue; and further, that the 
lecithin is relatively diminished and the non-phosphorised 
extractives increased on the left side. Although we cannot, 
in the absence of an exact knowledge of the chemical 
composition of the cord prior to degeneration, assert that a 
relative increase or decrease corresponds to an actual 
increase or decrease, yet, in view of the fact of the decompo¬ 
sition of phosphorised fats and of protoplasm referred to 
above (p. 347), it is not at all improbable that this is so and 
the probability is greater the more marked the variation in 
composition becomes. The change in composition found on 
the left side must be interpreted as indicative of a breaking 
up of myelin with its contained phosphorised fat and of 
axis-cylinder protoplasm. Turning now to the amount of 
phosphorus present in the two halves of the cord we find 
in both extract (2T4 per cent, against 172 per cent:) and 
residue ( 97 per cent, against 92 per cent.) but especially 
in the former there is a defect of this element on the para¬ 
lysed side, while a corresponding difference occurs in the 
total phosphorus in the two half-cords (138 per cent, right 
against 1T9 per cent. left). In this connection it maybe 
observed that one of us in a research published elsewhere 
has found in a perfectly healthy spinal cord from a case of 
death by accident 1*47 per cent, of phosphorous, and in 
spinal cords of patients dying from various affections free 
from degenerative changes, as revealed by Marchi and 
Weigert staining, the percentage of phosphorous is 1‘47 per 
cent, to T40 per cent. So that a certain degree of defect of 
phosphorus is present on the right as well as on the 
paralysed side, and reference to the diagram illustrating the 
degeneration found by Marchi’s method will show the reason 
of this. 

Turning now to the analysis of the spinal cord of Case 2, 
a reference to the accompanying table shows an essential 



agreement with the .preceding, though here the difference 
between the two halves is not so marked, and some points 
of divergence arise, the two cases not being strictly com¬ 
parable, owing to the existence some time previously of an 
attack of opposite hemiplegia, though, as far as the appear¬ 
ance of the sections is concerned (fig. 1), there is a consider¬ 
able resemblance between the two. Commencing with the 
percentage of phosphorus, it is to be noted that the half¬ 
cords contain 142 per cent, and l - 38 per cent, respectively 
on right and left sides, both halves thus being defective in 
this element, the left more so than the right. The right 
extract (193 per cent.) is richer in phosphorus than the left 
(T84 per cent.), but the right residue ('98 per cent.) contains 
a lesser percentage of phosphorous than the left, a point 
which will be referred to again immediately. The right 
proteid residue (53'4 per cent.) is less than the left (56*7 per 
cent.), and correspondingly the ether extract (46'6 per cent.) 
on the right side is greater than on the left (43*3 per cent.), 
though the phosphorus in the extract calculated as lecithin 
is defective on the paralysed side, the remainder of the 
extract, after subtracting the quantity assumed to be leci¬ 
thin, being 23‘1 per cent, on the right and 22'6 per cent, on 
the left side. The right half-cord contains 75'79 per cent, of 
water, and the left half-cord 75'19 per cent., a result which 
does not appear in the table. 

Contrasting these results, it is to be observed that the 
second cord agrees with the first, the differences between 
the two sides being, however, less accentuated, in the follow¬ 
ing points (see table): the percentage of phosphorus in the 
left half-cord, as also in the left etheral extract, is defective 
as compared with that on the right side; and the percentage 
of lecithin is also less on the left side (by 3'3 per cent, in 
case 1 and by 2'8 per cent, in case 2). The points of 
divergence between the two consist, in addition to the 
slighter degree of the differences on the two sides just 
enumerated, in the defect of residue on the right side of the 
cord of Case 2 (53'4 per cent, against 56'7 per cent, on the 
left side), accompanied by a corresponding defect in the 
percentage of phosphorus in the residue on this side ( 98 as 



against 1'03 on the left side, the latter number being higher 
than on the same side in the first case); and in the unusually 
high percentage of ether extract (46 6 per cent.) on the right 
side of the cord of Case 2, as compared with that on the same 
side in Case 1 (38’9 per cent.). 

Discussion of Analysis. 

As the two cords are not strictly comparable, the second 
having been injured by a previous attack of hemiplegia, 
some differences would of course be expected, but such as 
occur in the second cord are not in conflict with the 
changes found in the first cord, and points of agreement are 
to be found even where at first sight only points of differ¬ 
ence appear. Thus, while the right residue in cord 2 con¬ 
tains slightly less phosphorus than the left, in opposition to 
what is found in cord 1, nevertheless in both cords the side 
which exhibits the higher percentage of phosphorus exhibits 
also the higher percentage of residue ; in other words, it 
would appear that as wasting of the proteid material occurs 
a disproportionate wasting of the phosphorus-holding con¬ 
stituents takes place. Let us next consider the second 
point of divergence referred to above, namely, the unusually 
high percentage of ether extract on the right side in Case 2, 
which is in striking opposition to the proportion present on 
the same side in Case 1, there being on the other hand a 
substantial agreement in the percentages of extract and 
residue on the left side of the cords. That there should be 
a divergence on the right side in the two cases is to be 
expected from the history, and the extreme character of the 
divergence seems to be due to the fact that the degeneration 
during the longer period elapsing between the right hemi¬ 
plegia and the date of the analysis, has become more 
complete than that resulting from the second attack on the 
left side, which was of about a fortnight’s duration. We 
have, in fact, some of the changes seen on the left side 
present in an accentuated form on the right side as a result 
of the right hemiplegia. The increase in extract on the 
right side is seen on reference to the table to be due to that 
portion of the extract over and above the amount calculated 



as lecithin, which becomes augmented at the expense of the 
residue. Now, as protoplasm in degenerating gives up 
material staining with Marchi’s fluid, it might be supposed 
that this increase in ether extractive would be due to the 
formation of fat. That fat is formed in degeneration of 
nerve protoplasm (axis cylinder) is exhibited in fig. 2, where 
the axon is stained black, so that this process also must 
accompany lecithin degeneration in hemiplegia, but it does 
not appear that fat is the only extractive contained in the 
23T per cent, of extract over and above lecithin present in 
the right half-cord of Case 2, for if this were so the section 
of the cord stained with osmic acid would be nearly equally 
stained on the two sides, whereas the staining is much 
greater on the left than on the right. 

As just stated, it appears that when the proteid residue 
wastes, a disproportionate disappearance of its phosphorus 
occurs. The question naturally arises, where does this 
phosphorus go to? It must either be taken away by the 
blood-stream, or it remains behind in a form which is 
soluble in ether. In the latter case it would go to increase 
the amount calculated as lecithin, which would accordingly 
be too high. This probably explains why the percentage of 
lecithin is higher on both sides in the second case than in 
the first; and also in Case 1 the percentage of lecithin is, 
for the same reason, a little too high, and the actual loss of 
lecithin is probably greater than would appear from the 
number given. 

Another fact may be again referred to here. The right 
half of the cord of Case 2 has about 6 per cent, less trans¬ 
verse area than the left side, indicating that, as might be 
expected, an actual wasting of the cord occurs as the lesion 
grows old. This is the only direct evidence of an actual 
loss of tissue which we have been able to obtain. 

Beviewing these results, which place some of the altera¬ 
tions seen in sections of degenerated nervous tissue in the 
form of a quantitative chemical analysis, it will be observed 
that they are in harmony with our knowledge of the decom¬ 
position of phosphorised fats outside the body and of fatty 
degeneration of proteid material within it, and that they 



exhibit the breaking-up of phosphorised fat and of nerve- 
protoplasm in the spinal cord in hemiplegia, as well as the 
increase in extractives not wholly fatty, formed at the 
expense of the proteid degeneration. The first case being 
uncomplicated is much more readily understood than the 
second, which could not be easily interpreted in the absence 
of the knowledge gained from the former. 


The preceding observations may be summarised as 

A. On the degenerated side of the cord in simple hemi¬ 
plegia, it was found that—(1) A breaking-up of phosphorised 
fat occurs; (2) the amount of lecithin present is diminished; 
(3) the amount of fat present is in excess ; (4) the amount 
of extractives soluble in ether is increased; (5) the proteid 
residue diminishes in amount pari passu with the increase 
of extractives; (6) the phosphorus in the residue diminishes 
at a still greater rate than the residue itself; (7) the per¬ 
centage of phosphorus in the half-cord as a whole is dimin¬ 
ished ; (8) the ether extract has an appearance of butter 
instead of being crystalline. 

B. When two attacks of hemiplegia occurred, affecting 
in succession both sides, the alteration of composition of the 
cord was more complex, but was such as would be expected 
from the development of the changes above recorded in 
sequence in the corresponding half-cords. 

Description of Jig. 1, a, b .—Transverse sections of the 
spinal cords of Cases 1 and 2 respectively in the cervical 
region, showing the extent of the degeneration in the crossed 
and direct pyramidal tracts and elsewhere. R, right side; 
L, left side. X 4. 

A section of Case 1 shows by Marchi’s method marked 
degeneration of the left crossed and the right direct pyra¬ 
midal tracts. There is also some slight degeneration of the 
right crossed pyramidal tract, and a few scattered fibres are 
found degenerated in the other parts of the cord, particularly 
in the right antero-lateral descending cerebellar tract and 
the left direct pyramidal tract. 

A section of the eighth cervical segment of the second 



case stained by Marchi’s method exhibits a greater degree 
of degeneration than the previous section. The degenera¬ 
tion is most marked in the left crossed and right direct 
pyramidal tracts. The right crossed pyramidal tract 
exhibits a lesser degree of degeneration, and there are a 
few scattered degenerated fibres elsewhere, particularly in 
the right antero-lateral descending cerebellar tracts, and 
also in the left antero-lateral ground fibres and adjoining 
portion of the left anterior horn. The large cells in 
the right anterior horns in both sections contain black 
granules, while in the left anterior horns the cells are 
similar or more frequently are represented by much smaller 
collections of dark granules. 

When the two sections are compared together side by 
side they are seen to resemble each other very closely as 
regards the distribution of the degeneration, and there is 
little in Case 2 to suggest a previous attack of hemiplegia 
affecting the opposite side. The right half of the section 
of Case 2 is smaller than the left, the diminution being 
estimated at about 6 per cent. 

Description of fig. 1, c, d. —(c) Longitudinal section of 
spinal cord, sixteen days after hemisection stained by 
Marchi’s method. In several places degeneration of the 
myelin sheath is seen in the form of longitudinal masses 
of a deep black colour. In relation with these, several 
degenerated axis-cylinders are seen which, not being sur¬ 
rounded by degenerated myelin products, are seen as fine 
threads stained black with osmic acid. In many places also 
the degenerated products are seen arranged longitudinally 
in the form of a single row of black spherules. X 120. 

(d) Transverse section of the left crossed pyramidal 
tract of Case 1 for comparison with the preceding. The 
degenerated products are found to be black throughout, 

A. Noll, working in the laboratory of Prof. Kossel, has divided the sciatic 
nerve of a dog on one side. Fifteen days after the operation the animal was 
killed. The phosphorus in the degenerated nerve was 67*4 per cent, of that 
of the healthy side. The alcoholic extract of the degenerated nerve was, 
however, 77 per cent, of that of the healthy nerve. Referring to the above 
work Noll remarks: “Diese wiirde in Uebereinstimmung sein mit der 
Annahme welche die Englischen Autoren beziiglich der chemischen Vorgange 
im Molekiil des Lecithins geaussert haben.”— 44 Ueber die Quantitativen 
Beziehungen des Protagons zum Nervenmark,” von A. Noll. Hoppe-Seyler's 
Zeitschrift fur Physiologische Chemie , Band xxvii., Heft 4 und 5,1099. 

, arcoivks / : v- ; 

^ecvipyum more, than■llW space ongioaily occupied by tbe 
nerves before degeMeratKUi. X 120. 

) .z\n Rumx. Su?a, 


KOicr extract-. • Krittif-^xtraot... &<•£ • % 

/ : C^c^i^d !im:U*£U fcrt!t ^ • CtUcuiatftd lec-itiim - 

; tHher *3S*‘2 • ' Oitor 

' - • . Residue. :v&&v: 

' • . . 

PUpA’pboTu^'-i-ti otiKt? ey.irwi 3*72 IV, ■ ineib*>r 

, iittif-oovd 1*19 ,, fcilbcjtn:^ i^ . 

^ //. 

tUb^r; Extract... 48’3 %t Y ' YV' - Etheft extract ’ • M'&'&W : Sy ; v 

Otilo, as lecithin ..-' 30 7 V, Calc, a*# l&citlna »* 2^"- 

• extractives ,Y 22^0.^ Ot«b*r «fytrft.cU'v^.... YSfc; HlW 

Itesidue „. 56*7,, Hosiduo YiY . 

. • . . i .. .. . ■ . . , 

.strfoef* tfltrac&v 3 V 84 % Phosphorus it» ether extract 1*§8 ^ 
M ro&tdue 1-03 ‘V> .-, .. residue .. Wx, 

hftJfrCO^ J*88 . * ,.y ?r hftlf-cord' .. . i ' 4 %%' 


Y'Vy- 1 -'• : :: "; ••' Y' ' -V’■»' ;■ '"'“ • ‘ FxQ, ' . ; V'*' -.v/- • i 'i'.vv - 

.. r.>v-Sr. ••• ■.■ •. : •■• . • •- ■ '• - .'•;•• -,.... •..-•»?• t • ■ v .'.■»■ ■ ••;..• «•/ ».*V* ,;v -/■'•'- 7 , 

. -■ .... 

,'■ •: f '. 


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• • • • V. 



hditff*# ;-v 

Ta* i*! * 7 • - 7 ; 

, jHuj . J. 


:'I»iguili.^atipt., 4 Ai<un*U i> 

.. . - '^<»?JWV.VSS'a ' '-}V. ••>• •;>'? * v5wa»> • '* 

’■• *•* I!* ^* f : *. r • * r .. # . 

'• ; ■-' • v . ' :'; 


b. : v VV 

c : tY w 

. ■:. i-»a. ; • •; i ! 

7*~r. ; 

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120 diaroetero 

'' ; ; .. ■ 1 *iI '! :! it Iti'ji•;• : %l'ill*, 

; 7: Sl^iiP} il ■ 



BY F. W. MOTT, M.D., F.R.S. 

E. H., female, aged 83. Admitted to Claybury Asylum for general 
paralysis November 11, 1895. Unmarried ; occupation, general servant. 
She says that up to a year ago she had been able to do her work quite 
well. She then noticed that her hands became weak. Although her 
speech is thick and indistinct, she gives perfectly rational answers to 
questions. Her memory, she says, is not so good as it was, and she and 
her friends have noticed a progressive defect in her speech. She has a 
small head and large projecting chin, and this, taken with her lachrymose 
condition, gives her an imbecile appearance, although, on conversation 
with her, it is apparent that she cries because of her helpless condition. 
The pupils are equal and react to light and to accommodation. There is 
a marked wasting of the muscles of the hand and forearm, with a con¬ 
dition of main en griffe , rendering her quite helpless. The thenar and 
hypo thenar eminences are particularly wasted; also the interossei, 
She is unable to extend the fingers. The muscles of the body are 
generally wasted, but the shoulder muscles not in particular. The respi¬ 
ratory movements are mostly diaphragmatic, the upper part of the chest 
moving very little. There is a general wasting of the muscles of the leg. 
and a tendency to foot-drop and inversion. There is very marked foot- 
clonus, patellar clonus, and WTist-tap contraction obtainable. She has 
lost power over her sphincters, and she has some difficulty in swallowing 
and masticating her food. She protrudes the tongue with difficulty w r hen 
asked, and she cannot protrude it far beyond the teeth ; it is tremulous. 
There is no loss of sensibility. The muscles were tested with the faradic 
current, and responded; but a stronger current than usual was required. 
A systematic examination was impossible, owing to the patient’s 

November 26.—Patient is much weaker; bulbar symptoms much 
more manifest, both in difficulty of speech and swallowing. She is very 
emotional, and continually cries out for water. She still goes about the 
ward wheeled in a chair. The left pupil is rather larger than the right, 
but they react to light and accommodation. Her craving for water is no 
doubt due to polyuria, for she is always wet. 



January 29,1896. —Patient is much feebler and more helpless, muscular 
wasting more marked. Knee-jerks and wrist-tap contraction very exag¬ 
gerated. Can feel the lightest tactile sensation on the leg; can protrude 
the tongue between the teeth, but the speech is much more muttering 
and indistinct, although she seems to know what she wants. She is now 
unable to swallow even minced food. She passes a large quanity of water 
under her, which cannot therefore be measured. She continually asks 
for water. Her extremities are cold, and she is evidently sinking fast. 
A few days later she was affected with ulcerative colitis from which she 
died.—F. W. Mott. 


Muscles wasted; skull symmetrical, thick; dura mater slightly 
thickened; pia arachnoid somewhat opaque and thickened ; Pacchionian 
bodies numerous at vertex along mesial line; convolutions large, simple; 
sulci shallow; cortex small in amount, fair consistence, pink, striation 
marked; ependyma smooth. Cord —Recent haemorrhage round the dura 
in cervical region, the clot being dark and soft, extending from 4th 
cervical to 5th dorsal; cord soft, flabby, wasted in the cervical and upper 
dorsal portions. In the region of the lumbar enlargement it is much 
firmer, and there is no apparent wasting. Muscular tissue of heart very 
soft, brown, and small in amount; weight, 5 oz. Liver —89 oz.; slightly 
fatty. Spleen —4 oz.; firm. Kidneys —9J oz.; capsule slightly adherent. 
Large intestine congested throughout its entire length. Tw r o ulcers on 
the first part of rectum, one large, about £ in. in diameter, with thick, 
overhanging margins. 

Cause of death, —Ulcerative colitis and dementia of general paralysis 

Microscopical Examination. 

The brain and cord was preserved for me in Muller’s 

Staining by Weigert-Pal, Marchi-Pal, and Walters 
methods, showed the following changes:—Degeneration of 
the pyramidal system in the internal capsule, crura, cerebri, 
as well as in the pons, medulla and cord. Atrophy and 
pigmentary degeneration of the anterior horn cells, especially 
of the cervical enlargement. In place of the atrophied 
cells are large numbers of branched Deiter’s cells. The 
destruction appeared most evident at the base of the anterior 
horns. Atrophy and degeneration of the ground fibres and 
anterior roots corresponding thereto. No affection of the 
posterior column nor of the posterior roots, nor of the 
cerebellar, nor antero-lateral tracts. The examination of the 
medulla showed a complete atrophy of the cells belonging 

A . CASE (,*P AM VOrEpil'XrfC-. Sfil 

to the glossodafeiod&eytigeui nucleus, situated about the 
apex of tho calamus scvipturms. Partial degeneration and 
atrophy pf cells mfcheOtio 10th. lltb and ISlhUuclei above 
the point of the calamus, Other cranial nerve nuclei were, 
unaffected. By partial degeneration in ...meant' stage* 
front simple swelling and breaking' off of processes to dis¬ 
appearance of the body of the cell and Tcpiacvment by 
pigment. Considerable atrophy fibres 

were observed in the. ulnar nerve; also the small muscles 
of the hand examined by. Mar chi method showed fatty 
degeneration and atrophy. 

In a casH previously reported I showed that there niay bo 
an atrophy of the-large pyramidal cells of the Eolandic ayea 
(Mrmn, and thy following■ points..arc, I consider, of 

eSpectsdi int^tdsfe M this easey the cortex 

and £bt: cfirjjus callosum in thiecage was made by. the 
March? method- Great numbers of degenerated fibres were 
fowhd'iih both .{ibjsho^i .the; 

iho-rOMtCKOGaWH- ?> ;.:, . 

>>i ftfjAal) js^tfcfoii of tb* yorf' U;> •jaUoauni c^mosUn the sent n»t 
convolu.UUjts Tfjw fibrce Are cut tr»A«vor.?*y* atitl ^ eoU^iao'rab’e otiinfef M’i 
^ieii df^caxjmkU., iu<*atif large fibres. 

dygeneratipn found in the central, port?on of the. 
callmi/m. In will be observed that, the-large fibres; especially 
ave affected. It rhE^he^ suggested that this id my way proves, 
that i*.->».• se degenerated ftbres Lvave flu- hiuuc origin as the 
pyiiumdal fibres cif the internai ; capsule. I think, however, 
they have* lesions ..hf thh Eolandic 

ayeftiii animals have been showtito^ ptpduoe de-genaration in 
tins region (Mott, Muratow). Examination of the cortex 

W&- .UiCHIVI^ 

by ivIftrchi-Pa} method showed the tangential fibres in t in t 
ivi-Jf photomierc, ”2). The diagnosis of general .paralysis is 
; ?i(^-^'a«aWfc^;i,.6ioreoteie sections of the cortex stained by 
the Von Oruddeti carmine method showed degenerative 
atrophy, scattered, not diffused. of the third layer,/and also 
of the fourth layer of the cortex, but Jutie if tuiy change sn 
the. Superficial tangential layers.. ^his is hardly like general 
paralysis’; it seems more likely to. be a. primary’ systemic 
degenerative process affect ins: the efferent system of Deurons, 


H#ojt.fari of the cerebral cott&c, RioWn^fc'arc& i>f £iibe .of ftiny Atrophic 
l&ter&l bderasis stained by -)&lt£feirV Marhbi-IVd mashed: I\r4g»iflca,tum 
1$) ilf&iueters. ...' ’ 

and examiniition of these ^eetiohs repealed a pathological 

the spinal cord ; the large pyrtumd&l cells could bo seep, in 
vftfihhe stages of degenerative, atropbay their proeesses 
broken off, their sides £utved outwards, and goto* of the 

1.iy scattered foer /the..^ell^ybuys/niitinilly; dssfeppeajed and 
,: hraR£ib.ed':: eelf*. arte *een, ? s5.Vsiif&F m all respects , to 

those met with in the anterior horns (ejkfc photoniicxo- 


graphs y and 4). jp the subcorticalwhite matter there #0 
great numbers of branched gdlfe and staall round 
cells amidst atrophied and d€)^eu%afed hiyelinated fibres. 
The degenerative .process must have befeu a primary 

of neuron*, I could find no vascular change Vfbigh would 
in any wa;y account for the process,. ft did not affect the 

T’uotouic uouiu rn a. 

i'bntamicrogrftpli 3. Cells of the third layer, showing with 

processes broken Wioi> wiib. sidt-fi curved outward*.* T:ha excess o l 
plgUientatrox) i;s nat Section was stairvecT witl) Vpft 

caremae* TifBygi-ijficAii^u 300 d<Aj'n<ijier». 

association, systems of neurons, for the tahggutiiU supra- 
radta} and ipfe^radial fibres are intact, said ^htieoSof all 

N,B.-* Th;'. specimens were shown at a patUoiogiceij 
meeting of the Neurological Society:’; 1 have two other 
casesmusdnlir shortly be 

published, when remark* upon this and pi’evibusly recorded 
eases will be givga, ' \ - 

ARCXM\ Jift 

PHOwmcjaoGnAra 4, 

Photomicrograph 4, showing branched Dei tor 4 b cells iu the 
the cortex and absence of pmmid?il cells. Tho appearance presented c-orrstt- 
pondt-6K»ctly %yttb •wbat->?hld'&i >ha advanced di^aamthd phx^as 

met with in the anterior The^* advanced degerwrativfc conditions 

are not uoivetsal, but. occupy small foci in the deepest layer of tho cortex 
and subjacent yrhjte fn&Uer Magnification 250 diameters* 


BY F. W. MOTT, M.D., F.R.S. 

F. M., aged 5 months; admitted into Charing Cross Hospital on 
August 12, 1898. Bom full time, easy labour. Breast-fed until now. 
Appetite usually good, bowels irregular. Parents are both living and in 
good health. Eldest child died when 10 months old. Second child is 
healthy. Patient is the third child. Present illness began on Tuesday, 
August 9. At night the child woke suddenly, screamed, and appeared in 
pain. Mother had to nurse her in consequence, and in the morning 
brought the child to the hospital. 

August 9, 1898.—Patient had a temperature of 101°. Had been sick 
and had had bowels moved once or twice. Legs not paralysed. No 
assignable cause. Gave citrate of potassium and a mild purge. 

August 12.—Saw patient again. Mother said that the child’s legs 
were both paralysed. She noticed this the evening before. 

August 15.—Both legs paralysed, no wasting. Legs lay on bed in 
position placed. Plantar reflexes absent. Pain was felt on pricking with a 
needle, but no movements were elicited in legs or thighs. There was 
some slight spontaneous movement in all the toes of the left foot, and 
also in the fourth and fifth of the right foot. The child is quite cheerful 
and bright, taking food well. 

August 18.—Condition of legs, Ac., did not vary at all, the muscles of 
left leg became very flabby, and the sensibility to pain appeared increased, 
at least the child cried more readily. Electrical reactions were not taken, 
as the child developed intractable diarrhoea. 

August 25.—Diarrhoea increased with rise of temperature, and death 
occurred on 25th. 

Post mortem .—Nothing abnormal in viscera. No ulceration, Ac., of 
intestine. Spinal cord —Sciatics and their prolongations with portions 
of muscle retained for examination.—Abstract of notes by P. Daniel. 
House Physician. 

• 'C(i Alicmves 

of the Tissue* of Infantile 

■ -p- 

otrly the lower part of the atiil the 

sciatic nerves and their branches to the muscles were 
preserved by M£; IMiio], , ’> V/o/o f 

These were hardened in a mixture of MwUr.r ami ii per 
cent, formalize, equal, parts,. Sections weta afterwards cut 
in oeiktidub The s&hiingy method used being (Irfem’.s 
method for Micro-organisms. March! method, Weight- iron 
carmiiie and. camunt with subsequent polychrome hiue. 
This latter method shows, not only the 
also the axis-eyihjdev nrocesses. tor a long disfabwe, even 

also the axis-cylinder processes, for si lo; 
when they are swollen up and degenerated 


Vertical roctioii of the lumbar tavFaxgemortt of Um *phuii con}, jus>t 
behind the anterior median fisBurc and thro oghtbo anteriu r rainm i ^u re. 
soctiMj? -mined with carmine. On. either side of the mid line is w clear 
sjia-vC contRiniog. granular matter. This corresponds to the terraiitft] dt* 
triiiMinon of OfM< ni. tba- ' branches ^iveu oft >ju eHhuv hsidu hr Uic atrtggijgf 
ra^ii^ WUry at thebotfcom of the twute* MagnifioaUpn 12 

a-bcuit in the tissue, hut both irregular furai. and the distn- 
fcdtlh'U would, not allow one to assrune more than' an 
ttceidtmtai connection!. Thmtifirmth sifeiried pjtiticles,, which 

Obama met too, vxu 

mined with oil rum 

lnrsirm,. Mlhd,- id 


show any luicro-orgu 

m isms, which. 1 would 

v^OuUnt for the. . 

y it\} # v - -jf 

■ tntpOse inflammation 

observed in the awl 

ierior cornua. A 

certain number of j 

stained particles wot 

e seen scattered. 


might be micrococci, bore no relation in distribution to the 
inflamed blood-vessels. 

Carminate of soda preparations.—Vertical sections of 
the lumbar enlargement in series stained in bulk showed 
on each side of the central canal of the cord a vessel ending 
in a flask-shaped area of softening, due to inflammatory 
thrombotic stasis of two terminal branches of the artery 
which bifurcates at the bottom of the anterior median 
fissure {vide photomicrograph 1). 

Carminate of soda preparations subsequently stained 
with polychrome blue by Nissl’s method. Weigert iron and 
Weigert carmine exhibited the following changes:— 

(1) Mid-dorsal region .—Very little, if any, inflammatory 
change in this region. The cells of the anterior horn 
appear fairly normal, also those of Clarke’s column. 

A large number of fibres in the antero-lateral column, 
however, show their axis-cylinder processes swollen up and 
staining but faintly as compared with the normal. Strange 
to say, there are some likewise in the posterior roots, but I 
could find only one scattered here and there in the anterior 
roots at this level. 

8th dorsal downwards .—The inflammatory change in the 
anterior horn commences about this level and increases in 
intensity downwards; the inflammatory process, however, 
has not much altered the anterior cornual cells, for most 
of them show the granules of Nissl and their axon processes 
are not swollen up. The inflammatory process increases 
slightly as one proceeds downwards, being always more 
marked on one side than the other, but not until we arrive 
at the 1st lumbar is the inflammation so intense as to 
produce marked destructive and degenerative changes in the 
anterior cornua and to a certain extent, but much less, of 
the cells of Clarke’s column. 

Minute description of the appearance presented by (a) 
the vessels; (b) the cells; (c) the fibres at the level of the 
lBt lumbar segment downwards. 

(a) Vessels ; low power; 100 magnification.—All the 
small vessels, arteries, veins and capillaries in the anterior 
horns are surrounded with leucocytes and the whole of the 



nervous tissue is infiltrated with round cells and leucocytes, 
so that the nerve-cells are with difficulty recognised. Many 
of the transverse sections show little hollow spaces con¬ 
taining only granular detritus, with round cells and leucocytes 
around, evidently, little foci of necrosis. 

The ganglion cells, especially at the base of the anterior 
horns, are either destroyed or greatly obscured and altered. 
The membranes are not much affected, but at the level 
of the 1st sacral there is a round-celled infiltration, 
but not very marked, in the neighbourhood of the anterior 
roots. Many inflamed vessels can be followed into the 
antero-lateral white matter along the roots. The sheath 
of the artery entering the anterior median fissure is sur- 




• c 

4 * 

n * 


* 9 



4 * 



rS r < 


t 4 


S It <* 

"A * 




Pig. A. 

Small vessels of anterior horn in Marchi stained specimens, showing 
leucocytes containing black stained fat particles. Magnification 200 diameters. 

rounded with leucocytes and epithelioid cells. Some of the 
small arteries and veins of the anterior cornua show a clear 
space along the periphery of the vessels, probably dilated 
perivascular lymphatics. 

In Marchi-stained sections many of the small veins and 
capillaries are outlined by cells with fine black particles 
in their interior, and these are either leucocytes swollen up 
and containing degenerated fat particles or the epithelial 
cells undergoing fatty degeneration (vide fig. A). One sees 
exactly the same appearances in the capillary vessels of the 

M ICK*$$ 1 >i I NATION 01 ' THE SPINAL LOIill 3t>0 

brain %: acute paralysis TIr-. *11:110 also lie 

Occasionally seen in the perivascular lymphatic .sheath of 
the vessels of the aohf.ruit median fissure,. 

{/.>) CdU sCatfiAd by carmine Nisd method.-—' The cells iii 
the: 1 umbar eid-argesoeut w swolleu up ftntl wilt not take the 
stain, they are .consequently meoguiaed with difficulty. They 
show no granule*, being eud'omdy •steteed a >hilf bluish. grey 
.colour, ibstead of puipfe Tfe axis eylimfet Itfbcssses are 
swollen up finer Vane, se \ddc pbotousievo. v 2), stained the 

rnoTOMionoG kai*h & . 

n^rapif t >i U&r: of mrtwior oonm, showing c?s11h. vtfilb vark'oso 
•wsi*. o>*lUrdi^ ^nd ‘ntitamnurtion in tinstiitf awjutid* Magnilieatioirt. ZtoO 

v‘V/ ; - ‘ * * ' * ‘ ^ ^ * • *' T .■ *♦ \ 

-same as the nerve-cell, a dirty slate grey colour. Some of 
tin-: cells <}( the anterior horn at the level oi the 1st and 
•2nd lumbar am but little affected, and they show their 
protoplasmi? processes distmeiiy.' and '$&. hudy.-pf i th'e.- ; '0 > ti 
presents the mosaic appearance due to the normal 'arrange¬ 
ment, of'the. chromatic substfUice. These numiivi cells are 
situated at the ftp<k& <5f the anterior hom. Many of the cells 
of Clarke : s cobuno are degenerated at this level. 

if) Fibre*, — Sections stained by Weigm method, show 
Tjardiy any- of the due purple Gained network in tl*e anterior 
horn, contrasting markedly with the fibres passing from the 
pudterwr foots and posterior horns into tbciprhy matter, 



Sections stained by Marchi method, show a large number of 
degenerated fibres in the anterior commissure, ground fibres 
and root zone, the antero-lateral ascending tract and the 
direct cerebellar tract, but to a less degree. There is less 
degeneration in the posterior column, and it corresponds to 
the endogenous system of fibres. Goll’s column and 
Burdach’s column contain but few degenerated fibres {vide 
fig. B); moreover, it will be observed that in the figure of 
the 4th lumbar section that the median oval area of Flechsig 
is undegenerated. This supports Hoche’s contention that the 
fibres of this tract represent projections of cells in the upper 
part of the cord ; at any rate the fact that these endogenous 
fibres are not degenerated, points to their not arising from 
cells in the lumbar region. 

It will also be observed how very definitely the posterior 
internal triangle has escaped in the lumbar region. The 
degenerated fibres seen in the crossed pyramidal tracts in the 
dorsal region are probably mostly direct cerebellar fibres from 
Clarke’s columns on their way to the periphery of the cord. 

Sections of the internal popliteal nerve show by Marchi 
method considerable alterations in the fibres, but somewhat 
different to those obtained by experimental sections of the 
sciatic nerve, the breaking up of the myelin not being so ob¬ 
vious, and the black staining not so intense. In transection 
some bundles show many more black dots than others, like¬ 
wise in longitudinal sections; varicosities also are seen upon 
the nerve fibres. In transverse sections stained by Marchi 
method, examined with a high power, the transections of the 
nerve fibres present a very different and varied appearance. 
Some few appear black throughout; some appear granular 
throughout; a considerable number show no axial core but 
have a swollen appearance, with the myelin sheath stained 
greyish green. 

Sections of nerve bundles going directly into the affected 
muscles, after staining by Marchi method, were examined 
both in longitudinal and transverse section ; these showed 
considerably more fibres degenerated and the degeneration 
was much more obvious. Some of the small bundles 
contain a large number of fibres in which the myelin is 


• v:. 

7fh ,^*vrf. 

4th lumbar 
Ft*. B. 

«i6rta iii rabbits. The evteinive d'^neratiow is *aen in iho hnnb&r 

vegion It dov* not, however. ^(Tot:i. the py/ar^dal tmts nor f»tAV-h eohmm- 
in this, region ; moreover^ the po.4^nor internal fcrian^e^ah A Uu* ovsif area, 
of Fleclisjg have eVe&cul., ihoiti m 10 'dhutt ©tar "■ v 

■ V.'-v;:. - ,:>V;Voi'V:.v.. ; .- : :^'V; ’- : ;.’ .--X/; i ; ^:ycr 





'iT -2 aba i!’t vjbs 

broken up and black, but in tran«*v<st*e. section it c,o.ttid 

be |pg$ifr that ■«• considerable -number <>£ the fibres were inf- 
al&eied. Ditlbrent bupdfes showed a Atyriod number of 
• fibres' d^eixbratuS, ftncV this <iui£e ttgreer with wh&i was 
observed in fchb ineterior boru^llg 1^1 'the spinal cord, for 
hmtiy of the cells, hs We h&vft raided* p^e^ted the normal 
granules ol-."Nisst, flifcrefbre theic; atfisoiyfcder process could 

*' •’ t \U > 

Sections of the Ater-yes Were elso ■serifiaed by Strtebe 
method and presented the following appearances:-— The 


A small;^tii/i nerye in- Ar&mv*rf®' s.eoUoxt, efcahux* liy 

aj.a\vhi/ a-j’ ; ' cJegenettitecl fibres Gained black. 


a^fe-cylinileiA- wefo swollen .up, .some tune* broken, some¬ 
times absent; the myelin j$ m plates, stained blue, in 
place** red: . when the fatter; there often exist irregular 
stainedbeaps of acidophil substances, and sometimes these 
can be seen to consist of corpuscle?. The axis-cyliadcrsi are 
sometirnes pot stained the deep, brilliant blue that healthy 
fibres strain s l>pt we, at» dull; purple chldut^-cspecfftlly is 
this the case tv hen the irregidar sWulien axmi can b»* 
iMf^eryed^—either in an empty primitive sheath or sunottmled 


by red-staining myelin ; the nuclei of the sheath of Schwann^ 
are in many places undergoing proliferation, stained red and- 
are finely granular; the interstitial tissue contains numerous 
phagocytes and some of them contain black particles of fat 
stained by the osmic acid. 

Muscle-fibres stained by Marohi fluid show the following 
appearances:—Very few of the fibres showed distinct 
striation and many of the fibres are in an early state of 
fatty degeneration. 


Cases of acute polio-myelitis terminating fatally within 
a month are rarely seen, and only a few cases have been 
recorded in which a complete microscopical examination 
has been made. Charcot, in 1879, put forward the 
hypothesis that the disease was a primary parenchymatous 
degeneration of the nerve-cells and the changes in the 
interstitial tissue he looked upon as secondary. Pierre 
Marie, in his Lemons sur les Maladies de la Moelle, in 1892, 
first called attention to the vascular origin of the disease. 
Rogier and Damaschino examined more recent cases and 
looked upon the disease as a primary interstitial myelitis. 
In the year 1889 Rissler examined three very recent cases six 
to eight days after death and described accurately the changes 
met with in the ganglion cells and the interstitial tissue. 
He came to the same conclusion as Charcot, but he did not 
exclude the possibility that the same noxious influence acts 
upon the nerve-cells as upon the interstitial substance. 

In opposition to Rissler, Dauber and Goldscheider ex¬ 
pressed the opinion that anterior polymyelitis is an acute 
myelitis, limited to the areas of the anterior horns; Dauber 
found similar changes in the ganglion cells to Rissler; 
marked degeneration of the nerve-fibres corresponding to 
the affected parts and interstitial changes in the form of cell- 
infiltration of the vessel walls of the adjacent tissue. 

Besides the anterior horns, other parts of the grey 
matter were affected, such as Clarke’s columns; and Dauber 
concluded that the affection of the ganglion cells was due 
to chemical, perhaps even mechanical causes by compres¬ 
sion of the cells and interruption of their nutrient supply. 



It was, however, Goldscheider’s work that first proved the 
view expressed by Marie, that the peculiar morbid changes 
met with in polio-myelitis was due to the affection of the 
branches of the artery at the bottom of the anterior median 

Kadyi, in 1889, had shown that the anterior grey 
substance of the spinal cord is supplied by the anterior 
spinal artery, and from this, at the bottom of the anterior 
fissure, arise along its whole length central arteries, which 
bifurcate one branch running to the right and another to 
the left and then they pass into the central part of the grey 
columns. Here they divide into finer branches, taking a 
more or less horizontal course, ending in terminal arteries 
in the grey matter of the anterior horns and the base of the 
posterior horns. 

My case is of interest in that it shows when vertical 
sections are made through the grey matter in series that the 
areas supplied by these terminal arteries may undergo a 
complete necrosis owing to the inflammatory affection of 
the vessels on either side of the median fissure {vide photo¬ 
micro. 1). 

Another point of interest is that the cells of Clarke’s 
column were affected and a degeneration corresponding to 
the same was found in the direct cerebellar tract above the 
lesion {vide fig. B). 

A third point obtained by staining sections of the cord 
by Marchi method; one observes a degeneration in certain 
regions of the cord. 

(1) The posterior columns .—The endogenous fibres in 
the lumbar enlargement are clearly shown, and this is 
just the reverse of what is seen in tabes, but an 
interesting point in this degeneration is that a group of 
fibres which frequently remains undegenerated in tabes is 
in this case free from black points. I refer to the posterior 
internal triangle; it seems to show that the tract may be 
of exogenous origin and that the reason why it does not 
degenerate early in tabes is that it represents the axis- 
cylinder projections of a special group of spinal ganglion 
cells. The endogenous fibres of the oval area of Flechsig 


are also unaffected, tending to show that they have a long 
course from above. 

The black points in the posterior columns diminish 
as we ascend the cord, showing that these endogenous fibres 
are for the most part short commissural systems. As there 
was a marked inflammation of the base of the posterior 
horns (even more general than of the anterior horns) it is 
probable that these degenerated endogenous fibres arise from 
cells in this situation. 

(2) The antero-lateral columns. —In the lumbar enlarge¬ 
ment the degeneration is very extensive in the whole of the 
anterior half of the white matter. There are a few scattered 
fibres in the region of the pyramidal tract, rather more on one 
side than on the other, at the level of the 12th dorsal. These 
are probably degenerated fibres arising from the cells of 
Clarke’s column on their way to form the direct cerebellar 
tract, which is well seen as a definite tract at the level of 
the 7th dorsal; in fact, the whole margin of the antero-lateral 
column shows a massing together of degenerated fibres. 
Being at this level above the region of the inflammatory 
process of the anterior horns, they represent for the most 
part the ascending antero-lateral tract—the degeneration in 
the ground fibres of the anterior horns diminishes as we 
ascend, so that these long ascending systems of the 
antero-lateral column become more obvious. The ascend¬ 
ing degeneration corresponds very closely with that 
described by Singer and Munzer, obtained by clamping 
the abdominal aorta in rabbits. 

Lastly, the small vessels of the anterior horns in Marchi 
stained specimens show leucocytes containing black stained 
fat particles. 


(1) Rissler. “ Zur Kenntnis der Veranderungeu des Nervensystems bei 

Poliomyelitis anterior acuta/’ Nordiskt Medicniskt Arkiv. y 1889, bd. 

xx., No. 22. Im folgenden referiert nach den Angaben von v. Kahlden, 

Dauber und Goldscheider. 

(2) Kawka. Inaug. Diss ., Halle, 1889. 

(3) Preisz. A. gyermekhiidts bonetandhoz , Ovorsi Hetilap, 1890, No. 51-52. 

Refer, in Neurol . Centralblaat , 1891, 8 . 396. 

(4) Dauber. “ Zur Lehre von der Poliomyelitis anterior acuta,” Deutsche 

Zeitschr . /. Nervenheilk , 1893, bd. iv., s. 200-236. 



(5) Goldscheider. 44 liber Poliomyelitis; mit Anhang. Bencht uber die 

Schnittserienuntersuchung eines Falles von spinale Kinderl&hmung 
v. 0. Kohnstamm,” Zeitschr. f. Klin. Med., 1893. 

(6) v. Kahlden. 44 Dber Entziindtuig und Atrophie der Vorderbdrner des 

Rdokenmarks," Zieglers Beitrtige, bd. xiii.; u. Centralbl. f. Allgem. 
Pathol. u. pathol. Anat., 1894, No. 17. 

(7) Redlich. 44 Beitrag znr pathologischen Anatomie der Poliomyelitis 

anterior acuta infant/' Wiener Klin. Wochenschr., 1894, No. 16. 

(8) Siemebling. 44 Zur pathologischen Anatomie der spinalen Kinderl&h- 

mung,” Arch. f. Psych., 1894, bd. 26. 

(9) Kadyi. Tiber die Blutgefiisse des menschlichen Riickenmarks , Lemberg, 


(10) Bebnheim. 44 Des Poliomyelitis anterieures aigues, etc.," Revue de Med.. 


(11) Makike8CO. 44 Poliomyelite cbronique de l'adulte d'origine chemique," 

Progrls mid., 1898, p. 121, 143. 

(12) Marie, Pierre. Legons sur les Maladies de la Moelle, 1892. 

(18) Drummond. Brain, April, 1890. 

(14) Oharlwood Turner. Path. Trans., vol. xxv., p. 203. 


BY F. W. MOTT, M.D., F.R.S. 

Female , aged 45, suffering from gra/ve anaemia, pyrexia, followed by 
spinal symptoms, the most prominent of which were vomiting , 
pains in the abdomen and constriction , diarrhoea , retention of 
urine , o/ control of sphincters , numbness and tingling in the 

limbs, shooting pains , tenderness on pressure , contracture of limbs, 
deficient sensibility , Zoas o/ aercse o/ position in hands. Diagnosis : 
pernicious anaemia, with spinal symptoms. Duration of disease 
two months. Death due to cystitis and secondary infection. No 
signs post mortem of true pernicious anaemia. Degeneration of all 
the long tracts of the cord, with secondary sclerosis. 

I am indebted to Dr. Abercrombie, who asked me to see this case a 
few weeks before death, for kindly permitting me to make use of the 

H. P., aged 45, a widow employed as a household servant, was 
admitted to the hospital, under Dr. Abercrombie, September 8, 1895, 
for oedema and numbness of the legs, accompanied by sickness and loss 
of appetite. The complaint began with tingling of the fingers, and 
sensation of cold in feet and knees, followed three weeks later by the 
oedema. For considerable time past she had suffered with attacks of 
vomiting and nausea, and loss of appetite. Her father died of phthisis, 
aged 40, mother of senility at 71, one brother and one sister both alive. 
No history of rheumatism, syphilis or haemorrhages, only illnesses were 
measles in childhood, and slight attack, of small-pox at 16. Has not had 
hard work, and has always lived well. Has had no children, and no 
miscarriages, menstruation ceased finally at the age of 89. 

Condition on admission. —Appears well nourished, but anaemic, 
mucous membrane very pale, skin almost lemon-coloured, heart weak, 
apex beat can neither be seen nor felt, and there is a loud systolic murmur 
with accentuation of second sound heard over pulmonary orifice ; murmur 
can be heard all over chest, but not conducted into axilla, venous hum 
at both sides of neck, most marked on right, veins of neck much 
enlarged and pulsate with diastole, also a marked pulsation in the neck 
just above manubrium. Pulsation of abdominal aorta is very obvious. 
Masses can be felt in right iliac fossa and across epigastric region, much 
less after enemata, no pain in abdomen, edge of spleen can be felt 



below costal margin, area of dulness increased, edge of liver not felt, 
area of dulness increased, respiration normal, urine neutral, 1008, no 
albumen, no sugar. 

September 3-10.—The patient was troubled more or less with head¬ 
ache, the bowels were constipated, there was some oedema of the feet; 
the urine was darkish, of low specific gravity, of neutral or acid reaction, 
with either no albumen or only a very faint trace. The blood showed 
1,700,000 red corpuscles to the c.mrn., and white in the proportion of 1 to 
130 red, with a small number of microcytes. 

September 11.—Pain and tenderness in legs, also in right iliac fossa, 
no deep tenderness over bones, but tenderness on pressure of nerves ; 
burning and shooting pains in arms and legs, sense of constriction around 
waist; put on liq. arsen., ni iij. t.d.s. 

September 18.—Attack of vomiting, pains in arms and legs, feeling of 
numbness and coldness in the extremities, with tenderness on pressure. 
Red corpuscles reduced to 24 per cent, of normal, white corpuscles 
six times normal. Retinal haemorrhages described by House Physician; 
sensation not tested; evidently the case was not considered to be a 
nervous one. 

September 17-25.—Shooting pains in the abdomen, numbness in 
anns and legs, diarrhoea has now replaced the constipation previously 
noted, poikilocytes noted in the blood, marrow tabloids ordered. 

September 27.—Gastric distention, loss of control of bladder and 
rectum, fresh retinal haemorrhages, one large haemorrhage below the disc 
of the right fundus. The corpuscles number 1,400,000 per 

October 8.—Diarrhoea and vomiting ceased, retention of urine, disten¬ 
tion of the bladder, and dribbling, catheter passed. The temperature 
since admission was raised a few degrees above normal the whole time, 
and varied from 99° to 102°. 

October 0.—Rigor, temperature 105°, probably due to cystitis and 
secondary infection Notes state there is a band of pain around the 
abdomen with shooting pains down the legs. Curiously enough, the 
notes state nothing abnormal made of it. Apparently it had not occurred 
to the House Physician that these pains were due to a nervous affection. 

October 7-14.—Worse again; yesterday afternoon (October 8) had a 
rigor, temperature 105°, after fifteen minutes sponging 101*6°, then to 
normal: takes food badly: the anus is very patulous; stools passed 
sometimes in pan, sometimes involuntarily: much faeces in rectum: 
micturition always by catheter. 

The nervous symptoms are now much more marked: there is 
much cedema of feet and legs: she cannot change her position in bed 
without assistance: can move thighs on trunk, but her legs are flexed 
and if forcibly extended return to their flexed position: her arms are weak, 
and she cannot hold anything, though her grasp is not much affected: 
she has a bedsore over the sacrum, and others threaten to form on the 
heel and great toe, and wherever there is pressure: one has formed on 
the right knee, through one leg resting on the other: she has girdle pains 
and shooting pains in the legs and arms, with tenderness: she can feel 
contact, but cannot localise it: legs feel like blocks; deep reflexes are 



increased: knee-jerks are excessive: increased patella reflex, and ankle 
clonus in both legs, also tremors: reflexes are slightly present in left arm. 

October 15-22.—Takes food tolerably well, but breath offensive: 
tongue furred, red and dry: sordes on lips and teeth: some diarrhoea: 
the urine is foetid and contains pus: bladder washed out with boracic 
solution twice daily: rather less oedema of legs: commencement of 
muscular wasting, especially in the arms: there are no new sores, but 
the old ones are rather worse: can extend legs rather more: there is 
marked sensibility to pain in the arms: common sensation is normal 
above elbow, but impaired, and incapable of localisation in forearm; loss 
of sense of position: cannot touch nose with eyes shut: great tenderness 
with increased reflexes in the limbs. 

October 23-28.—Much worse and weaker: breath offensive, tongue 
red and dry: restless from pain: face drawn : cheeks sunken: sordes on 
teeth and lips: violent burning pains in abdomen and back: stools passed 
involuntarily: bladder washed out twice daily: arms getting rigid and 
movements feeble and inco-ordinated : can only move fingers with pain: 
legs straighter, and there is some return of voluntary movement: the old 
bed sores are worse: there are no new ones, though some threaten: 
periodical girdle pains and shooting pains in arms and legs, also in chest, 
though the respiratory movements are unaffected: the wrist-jerks are 
exaggerated: pupils equal and react to light and accommodation. 

October 29-November 3.—She is now’ obviously sinking, and takes no 
notice; face is more pinched and cheeks sunken; pulse can scarcely be 
felt at the wrists ; tongue dry and brown; urine dark purple, containing 
much blood; her arms are drawn rigidly to the chest; no new bedsores. 
She gradually sunk and died five days later. 

Post-mortem appearances (described by Dr. Hunter).—Body ema¬ 
ciated ; rigidity slight in arms, less in legs, which were inverted with 
some retraction of adductor muscles; skin pale, not obviously cedematous; 
pupils equal, somewhat dilated ; no conjunctival jaundice; bedsores over 
sacrum. Thorax —Right lung adherent slightly, otherwise nothing 
noteworthy in respect to respiratory organs. Pericardium normal, 
contains a little clear serous fluid. Heart weighs 9 ounces, and con¬ 
tains a quantity of dark fluid blood; both ventricles contain clots; the 
valves are normal in size, and there is no ulceration or vegetations; 
the muscle is not obviously pale and certainly does not appear fatty to 
the naked eye. Abdomen —The liver projects one inch below the costal 
margin ; gall-bladder distended by pressure of contained bile; common 
bile duct and cystic duct much dilated, about the size of a lead pencil. 
Duodenum contains a large quantity of bile-stained mucus. Liver — 
Weight 60 ozs; lobules well marked on the surface, the organ on section 
appears somewhat fatty, and the smaller bile ducts are in part stained 
by the secretion. Spleen —Weight 5$ ozs., with a small adherent 
supernumerary organ ; it is firm rather than diffluent. Kidneys weigh 
together 9 oz.; pale and somewhat fatty. Bladder —Constricted; walls 
thickened; mucous membrane swollen and congested. Stomach and 
Intestines —Mucous membrane somewhat injected throughout; other¬ 
wise normal. Reproductive Organs —Normal. Brain —Increase of 



subarachnoid fluid and some flattening of the convolutions; vessels 
appear healthy. On section of the organ in various regions there is 
apparently increased vascularity ; otherwise normal. The brain, spinal 
cord, and some of the peripheral nerves were preserved in Muller's fluid, 
with the exception of some small pieces which were placed in absolute 

The marrow of the bones was examined by Dr. Hunter and found to 
be normal. The liver did not give the free iron reaction with ferrocyanide 
of potassium solution acidulated with hydrochloric acid. The heart did 
not yield evidence of fatty degeneration when treated with osmic acid. 
It may, therefore, be concluded that these faots, combined with no 
diminution of blood apparent in the vessels, disposes of the idea that it 
was an ordinary case of pernicious anemia. 

Microscopical Examination of Tissues of Nervous 


Small pieces of the cortex cerebri, of the liver, spleen, 
kidneys and the 4th lumbar and several other spinal 
ganglia were hardened in an abundant quantity of abso¬ 
lute alcohol. The spinal cord, the medulla, the lower 
part of the pons and pieces of the central convolutions of 
the brain, together with the ulnar, sciatic and median 
nerves, were hardened in an abundance of Muller’s fluid. 
Pieces of the heart and diaphragm and other muscles 
were placed in Muller’s fluid. 

When . thoroughly hardened the tissues which were 
placed in alcohol were cut in celloidin; the sections of 
the brain and spinal ganglia were stained by Nisei’s 

The sections of the liver were placed in a solution of 
ferrocyanide of potassium and acetic acid; they did not 
give the free iron reaction. The sections of the spleen and 
the kidney were similarly treated without result. The 
sections of the kidney stained' by Gram method showed 
septic foci and numerous micro-organisms; none could 
be found in the spleen or the liver. The sections of the 
spinal ganglia {vide plate V., fig. 2) were treated by Nissl’s 

The tissues hardened in Miiller’s fluid. Sections of the 
heart were stained with oBmic acid and pieces of the 
heart were placed in Marchi fluid. No fatty degenera- 

Plate V. 

a :;,v 45* 

#> .- k ^f4$5ari*. w * s 

<•’;•• ^-4 

p/ * ._** •’ ' * *^7 


Fig. 1. 

Section of third lumbar posterior spinal ganglion, from a case of very marked 
pernicious atneraia in which there were no cord lesions. Magnification 150. 

Fig. 2. 

Section of third lumbar posterior spinal ganglion, from a case of combined 
sclerosis with grave anaemia. Magnification 150. 

7\> /ace j 3 . 

' • "■ ^ ; ■ 

; ' r: 

John Half, Sou* <t Pcmteteon, Ud*, I/Hidon % W 


tion was found, nor was there fatty degeneration of the 
diaphragm. The muscle-fibres showed indistinctness of 
striation, as if there were commencing coagulation necrosis, 
and throughout the substance there were minute haemor¬ 
rhages and inflammatory changes round the vessels, indi¬ 
cating haemorrhagic myocarditis. 

Peripheral nerves (sciatic and ulnar).—Longitudinal and 
transverse sections of these were made after embedding in 
celloidin and stained by Weigert and Pal methods (unfor¬ 
tunately, the tissue was obtained some time ago and trans¬ 
ferred to spirit, so that the Marchi method could not be 

Sections stained by the methods above mentioned did 
not show much degeneration. One bundle in the sciatic 
nerve appeared to be sclerosed but it may be that this 
particular bundle consisted mostly of vaso-motor fibres. 

Sections of the spinal ganglia stained by Nissl method 
showed the cells only faintly stained; they are more pig¬ 
mented than normal as compared with the cells of a spinal 
ganglion in a case of pernicious anaemia ( vide plate V., 
fig. 1); but the changes can in no way account for the 
degeneration of the exogenous fibres in the posterior columns 
of the spinal cord. The examination of the spinal ganglia 
* was not systematically conducted, and too much reliance can¬ 
not be placed upon these observations alone. A number of 
posterior roots in the dorsal region were teased up and 
stained in Van Giesson’s fluid. All the fibres showed 
normal axis-cylinder processes, thus contrasting markedly 
with the continuation of the same in the posterior column. 

Sections of the spinal cord and roots were made at 
different levels. In the upper part of the lumbar enlarge¬ 
ment and at the 4th and 5th lumbar it was noticed that 
very many of the posterior root-fibres appeared quite 
normal, also the anterior roots. There was, however, very 
extensive systemic degeneration of the exogenous tract of 
the posterior columns, as in tabes, the endogenous systems 
more or less escaping; thus we find little or no sclerosis 
in the median area of Flechsig, the cornu commissural 
zone and the postero-internal triangle of Marie. Lissauer’s 



- ' . .<• >•*-' .,* ..... 

!'U, 1 

AfoKsot eoniplaie^ ^H'mfjwrfisjUivd kWitl Partial ^atterod degftii^at^m Jauit flatted 
Variuu* Ioval.-) of the cord .vod *iuH» from & mn&'tif convhihed iu >>*ive ao*<-nri,->; ♦ •. 

witVi an Cdiw^Or pnd'Vfcroti af»i/arut.»i* &.oci redo;* J t*r utpmiU Vw*< 

cosiBfMEp., wn u a&kmu .; 

tract, imimftm, docs iiipfc appear to by much affected The 
pj’raiiWfial ,fer»t<5te;'.'mi both sides are completed} 1 solm#ich 
The' process me* too acute to lead to shrinkage ; there 
appears to. be anovergrowth of glia JHibstance in place, of 
the atrophied nerve-fibres, and rlucre are a largo number nf 
congested vessels with Soiocwhnt thickenc-t! hyaline: avails 
in . the sclerosed area*. The anterior bom cells m.-this. 
regiou and the gtev mutter generally, show no sign:, of 
myelitis. There secnis, liowcveo fcp lie % great diminution 
of tine, myelinated fibres iri the anterior and pnsieiioi. 
lion), o oimpimal with the normal. 

tbe -piuaj tru'd hoau, a case <rf c< ■nikioMl' .icJeerhdK'. Wcigert 
method. MjJ dcciHi region, MA£iiii 1 «»tioa fr <U»ntet«r.-> 

Lower dorsal reywji 

The dcgenojrAtioiv affect! nearly 
the whole of Thepogtoiitif; columns, the cm^scd pyratnifla), 
direct pyramidal, ami the antero-laicral tracts. . The only 

fibres u£ the skmy>; ,*>> 7 ’ ' - . 

Mid dorsal.-dShorn a. li.ttfe less dcgvneniu.m m the 
posterior colo.mK»,"-bht; 'Mere -murked m tin- lateral owing to 
fUe degenerated direct cerebellar tr&ct appearing. 



Upper dorsal. —The complete sclerosis is less marked, 
pointing rather to the affection being less severe in this 

Cervical region. —There is complete sclerosis of the 
posterior median columns, partial of the postero-external 
columns; complete sclerosis of direct cerebellar, and par¬ 
tially complete of antero-lateral (probably the whole of the 
ascending fibres destroyed, judging from the degeneration of 
this tract in the medulla). The crossed pyramidal system 
shows less degeneration than below. The. direct tract on 
one side is pretty considerably sclerosed. 

Medulla and pons. —Sections were examined after stain¬ 
ing by Marchi method and by Pal and Weigert methods. 
Par less sclerosis was observed in these structures than in 
the cord, but still, in the long tracts mentioned, namely, 
crossed-pyramidal, ascending antero-lateral and cerebellar 
tracts, degeneration could be observed by the Weigert and 
Pal methods, though very much better shown by the Marchi 
method. No degeneration of the arciform fibres or of the 
fillet was observed, and the pyramidal degeneration could 
not be traced higher than the lower part of the pons. The 
fibres of the antero-lateral and direct cerebellar could be 
traced high up—the latter into the cerebellum ; and no 
doubt the antero-lateral could have been traced to its desti¬ 
nation had the material been preserved. Unfortunately, the 
upper part of the pons and the crura cerebri had been 
destroyed in making the post-mortem. 

Examination of the cortex cerebri. —Marchi method 
showed no degeneration in the projection fibres of the pyra¬ 
midal cells. 

Remarks on the Case and the Microscopical Exami¬ 
nation Detailed above. 

Many cases of spinal cord degeneration have lately been 
described as occurring in pernicious anaemia, but some of 
these cases which I have heard related and read of, appear 
to me not to be of that form of pernicious anaemia which 
Addison described, and which present a group of clinical 


symptoms the cause of which is at present unknown, but 
taken together form a sufficiently distinct entity to constitute 
a true disease per se. 

The two cases recorded by Dr. James Taylor were 
thought by him to be pernicious anaemia, although I believe 
he has recorded them now as associated with grave anaemia. 
This is much more likely, and there is no doubt in this case 
an associated grave anaemia occurred, but for the following 
reasons not the pernicious anaemia of Addison. 

There was no evidence during life forthcoming that 
nucleated corpuscles existed in the blood. The skin when I 
saw the patient did not present the old wax appearance. 
The urine was not high-coloured. 

At the post-mortem there was far too much blood in the 
body ; there were no changes in the bone marrow; the liver 
did not give the iron reaction, and the heart showed no fatty 

The degeneration of the long tract system is very difficult 
to explain ; for the most part the degeneration affects the 
cord particularly. It will be observed that the distribution 
of the areas of absolute degeneration is singular. The most 
marked affection is in the mid-dorsal and lower dorsal 
regions. This is of interest, seeing that vomiting was an 
early symptom, and that girdle sensation was later a promi¬ 
nent feature of the case ; but she came in with tingling and 
numbness in the fingers and swelling of the feet. It will 
be observed that the pyramidal degeneration is complete in 
the dorsal region, but above this it is only partial, and 
diminishes in intensity the higher we go. The antero¬ 
lateral and direct cerebellar tracts are degenerated through¬ 
out their course. The posterior columns are very extensively 
sclerosed, especially the long fibres which occupy the median 

We may consider this a cord lesion, the character of the 
degenerations and the tracts affected show this. 

Is it caused by a toxaemia or is it due to a vascular 
change ? 

The arguments in favour of the former are : the lesions 
resemble very closely those which have been described 




in other cases of grave anaemia, pernicious anaemia and 

There are, however,-several reasons why the toxaemic 
theory is not entirely acceptable. Firstly, there is no 
reason why a poison circulating in the blood should limit 
its effects to certain structures in the spinal cord and 
spare others, especially when the exogenous fibres which 
are degenerated in the posterior columns are not affected 
in the posterior roots. At the same time, the changes 
discoverable in the vessels in transection in this case 
were quite inadequate to explain the degenerations. It 
is possible, however, that the vessels which run in the 
long tract systems have different anatomical relations to 
those in the grey matter and the short systems. It is quite 
clear that the most intense affection is in the dorsal region, 
and if the lesion is due to failure of the vascular supply the 
process commenced in this region (the region in which 
meningo-myelitis is so common). The vascular supply of 
this region of the cord is most precarious. 

It is quite probable that the vessels in the white matter 
have a much less perfect anastomosis than in the grey 
matter, consequently a failure of the blood which comes 
from above and that which comes from below to reach the 
mid-dorsal region might suffice to cut off a segment of the 
cord from blood. Owing to free capillary anastomosis and 
much greater vascularity, the grey matter at that particular 
segment might suffer very little or not at all, while the long 
tracts might be so extensively damaged as to undergo 
degeneration. This explanation, however, is inadequate, 
because we find a considerable though scattered degenera¬ 
tion in the pyramids of the medulla. No doubt these 
degenerated fibres represent only the leg fibres, the de¬ 
generation is scattered, and there is little sclerosis because 
they are mingled with the healthy fibres supplying the upper 
part of the body. This explanation would be the most 
acceptable if we consider the lesion a vascular one. Even 
then we should be advancing a theory which is contrary to 
experimental experience, namely, a Wallerian degeneration 
backwards towards the trophic centre. We found no evi- 



dence of this backward degeneration towards the trophic 
centres in the posterior spinal ganglia, for, although there 
was complete sclerosis of the posterior column in the mid- 
dorsal region, the posterior roots in that situation presented 
no marked abnormal characters. 

The other view, that it is a toxic influence which has 
destroyed the long tracts by a progressive decay, also offers 
some difficulties in the acceptance, for it is strange that the 
degeneration should be practically limited to the spinal 
cord, particularly of the dorsal region, not affecting the 
posterior roots, as we know it does in tabes. Possibly it 
may be a combination of toxaemia and circulatory disturbance 
in the spinal cord. The symptoms began in some respects 
like dorsal tabes, and the fact that the pupils were not 
affected, the knee-jerks exaggerated, shows that there is 
a close relation between this condition and ataxic paraplegia. 
In fact, the examination of a case of ataxic paraplegia which 
died in the asylum, which I have not completed, shows the 
same lesion of the cord. That it was not a general vascular* 
affection in the nature of a diffuse myelitis is proved by the 
fact that the grey matter had for the most part escaped, and 
the vessels, beyond congestion and some thickening of their 
walls in the sclerosed tracts, showed no inflammatory 

The sections of the spinal cord in this case closely 
correspond w’ith the photographs of Dr. James Taylor's case 
figured in the last edition of Gowers, in which there is 
a very good account of sclerosis from toxic blood-states, and 
references to recent literature which I append. 

Tuczek. Klinische u. Anatomisclie Studien iibcr die Pellagra , Berlin, 

Belmondo. Riv. Speriment, 1839-90, xv. and xvi. 

\V illiamson. Brit. Med. Journal , 1894, p. 398. 

Lichtheim. Neur . Cent., 1887, p. 23G. 

Minnich. Ibid., 1889, p. G62. 

Charite Annalen, 1891. 

Muller. Inaugural Dissertation, Berlin, 1895. 

Dent. Med. Wochenschr., 1892. 

Arch. f. Psych., xxv., 1893. 

Brain, 1894. 

Med.-Chir. Trans., 1895. 

Brit. Med. Jour., 1897. 

Lancet, 1898. 

Journal of Nerv. and Ment. Diseases , 1891. 


The Laboratory, Claybury Asylum. 


E. B. was admitted to Claybury on October 18, 1893. 
She was 28 years of age; was married. She died on June 3, 

The following clinical history was obtained from the 
asylum notes, and is, unfortunately, scarcely as complete as 
might be desired. When admitted she was dirty in her 
habits, rambling in her speech, and had many delusions, of 
which the chief was that she was “ Jack the Ripper.” She 
was said to have been in this condition for three weeks. The 
tongue was furred and tremulous, the gait feeble, the pupils 
were unequal and sluggish, the reflexes absent, and the 
patient, who was deaf for four and a half years, was said to 
have had aural hallucinations during the last four months. 
There was an undoubted history of alcohol. There is no 
note with regard to syphilis, miscarriages, or the birth of 
children. She is said to have had previous attacks of mania. 
There is a family history of alcohol, but none of insanity. 
Her further history in the asylum is as follows: She im¬ 
proved somewhat at the end of nine months, but in August 
of the following year she had another attack of excitement. 
In July, 1896, her pupils were described as unequal, her 
knee-jerks absent, her tongue tremulous, and her condition 
as “ rheumatic.” In June, 1897, there is a note to the effect 
that the patient had had retention of urine for two days, 
that she suffered from shooting pains in the legs, that her 
gait was unsteady, and that she had Argyll-Robertson pupils. 



A note made after death, but referring back to October, 1898, 
describes an attack of vomiting which was followed by 
cystitis; the latter disappeared in a week or two. Loss of 
muscular sense was observed; there was no optic atrophy. 

Immediately after death the body was placed in the cold 
chamber, and the post-mortem carefully performed 19 hours 
after death. The body was wasted, post-mortem rigidity 
was present, the skull and membranes were normal; there 
were no adhesions of the dura to the other membranes; the 
brain weighed 1,170 grins., and was normal in appearance. 
Large tubercular deposits and cavities were found in the 
lungs; the heart was normal, the kidneys contracted and 
granular, and their capsules adherent; the bladder was 

The spinal cord was hardened in Muller’s fluid for eight 
months; portions were stained in Marchi’s fluid; the re¬ 
mainder was cut in celloidin and stained both by Weigert’s 
method and Pal’s modification. The entire cord was smaller 
than is normal, and in the cervical enlargement notably 
flattened dorso-ventrally. 

Throughout the cord sclerosis was observed in the pos¬ 
terior columns, whilst those sections stained by Marchi 
showed in addition considerable recent degeneration. This, 
however, is not entirely limited to the posterior columns, 
and its distribution will be referred to later. 

Degeneration and Sclerosis of the Posterior 


Lissauer’s zone is entirely sclerosed in all sections of the 
cord in the region of S. 3 to D. 9. From D. 9 to D. 1 it is 
only partially sclerosed, whilst in the region of C. 8 it is 
again completely sclerosed, the atrophy becoming pro¬ 
gressively less marked, however, in the regions of C. 5, 4, 3. 
Lissauer’s zone in the sacral region seems to be limited to 
that portion of the lateral column which overlies the sub¬ 
stantia gelatinosa of the posterior horns. In the lumbar 
region Lissauer’s zone is seen to extend into the posterior 
columns; this portion of the zone is readily seen in sections 



prepared by Weigert’s method. In the region of D. 10 a 
trace of the posterior extension of the zone can be seen, 
whilst above this region it is not met with again till the 
region of D. 1, where it is partially sclerosed. Above this 
point degeneration in this tract is not evident. It will be 
seen therefore that on either side of the incoming nerve-root 
there is sclerosis, due to the atrophy of Lissauer’s zone. 

In the posterior columns themselves there is a degenera¬ 
tion and sclerosis which is variable in quantity and position. 
In the regions of S. 2 and 3 there is a partial sclerosis of the 
root zone, that is, of that portion of white matter lying 
nearest to the posterior horns, but not extending ventrally 
for more than two-thirds of the dorso-ventral extent of the 
column. In S. 1 the sclerosis has increased and has spread 
mesially, but does not reach the median septum at any point 
except at its ventral limit. In the regions of L. 5 and L. 4 
similar changes are seen. In the region of L. 3 the sclerosis 
does not reach to the periphery of the cord as it does in 
segments lower down. In the region of L. 2 there is a 
concise and well-marked area of sclerosis reaching to the 
mesial septum in its middle two-fourths, and extending out 
laterally almost up to the incoming nerves. At the level of 
the 12th dorsal nerve the division of the posterior columns 
into those of Goll and Burdach begins, and here is seen a 
definite sclerosis in the base of Goll’s column, whilst ex¬ 
tending through the apices of Goll’s into Burdach’s columns 
is a large club-shaped patch of sclerosis, not reaching, 
however, laterally so far as the horns, and not intimately 
connected with the dorsal patch in Goll. In the regions of 
D. 10 and 9 the degeneration in Goll’s columns increases, 
apparently at the expense of that in Burdach’s column, 
where in this region the degeneration is quite small. In the 
region of D. 7 the degeneration in Burdach’s column again 
increases, and from here to the region of D. 4 it extends in 
a dorso-ventral direction, spreading at the same time laterally 
and involving the root zone. At the level of the 1st dorsal 
nerve the sclerosis in Burdach’s column is definitely in¬ 
creased, and extends dorsally to the periphery, whilst that 
in Goll’s column is a trifle less than that present in the 


region of D. 4. At the level of the 8th cervical nerve 
the root zones are markedly sclerosed, whilst there is a 
very definite patch of sclerosis in the dorso-mesial angle of 
Burdach’s column. At the level of the 8th cervical nerve 
the sclerosis in Goll’s column is limited to the base, that in 
Burdach’s is diffuse, and involves almost the entire column. 
In the region of C. 4 this diffuse sclerosis is more concen¬ 
trated, and approaches the mesial border of Burdach’s 
column. In the region of C. 3, in addition to the concrete 
masses of sclerosed tissue at the base of the column of Goll 
there is a considerable amount of diffused sclerosis towards 
its apices, whilst the sclerosis in Burdach’s column is much 
reduced, almost vanishing at the level of the 1st C. nerve, 
where, indeed, the degeneration present is concrete and 
limited to the dorso-mesial angles of Goll’s columns, some 
diffuse sclerosis being still present in the column of Burdach. 

In the medulla sections stained by Marchi’s method show 
a scattered degeneration in the nuclei of the posterior 
columns, whilst the contiguous nucleus of the 12th nerve 
is altogether free from degeneration. 

In the regions of S. 3 and L. 3 (diagram I., figs. 1-6) the 
sclerosis does not extend in a dorso-ventral direction for 
more than two-thirds of the extent of the septum, thus 
leaving the ventral third of the posterior columns untouched. 
In regions above the 2nd L. nerve the sclerosis extends in 
an anterior direction on either side of the median septum 
and occupies the position which was free from sclerosis 
lower down. In this case, therefore, the cornual-commissural 
tract (Marie) is unaffected. 

A reference to diagram I., figs. 1-10, will show that in the 
posterior columns, in regions from S. 3 to L. 1, there is 
a well-marked oval area situated about the mesial septum 
into which no sclerosis extends. This bundle occupies an 
increasingly larger and more ventrally placed area as it 
ascends till it comes to a more or less abrupt end in the 
region of D. 12, whilst at the level of the 10th S. nerve no 
trace of this oval area is seen. It appears, therefore, that 
in this case the septo-marginal tract (Bruce and Muir) has 
remained intact. 



In all regions of the cord under examination the dorso¬ 
lateral angles of the posterior columns is unaffected, excepting 
where the mesial extension of Lissauer’s zone is involved, so 
that the dorso-marginal tract (Westphal) is not involved in 
the sclerosis of the posterior columns. 

In reviewing the degeneration of the posterior columns, it 
is seen that the volume of sclerosis in the lumbar and cervical 
regions bears a definite relationship to the position of the 
limbs, and that this local increase contrasts strongly with 
the steady influx of degeneration seen all through the 
trunk region of the cord. The relatively small number of 
fibres which ultimately reach the nuclei of Goll and Burdach 
is well shown in figs. 1 to 20. The distribution of the 
sclerosis is, moreover, of considerable interest from the point 
of view of the non-involvement of endogenous tracts in tabes, 
which has been urged by Mott and others. 

Further Degeneration in the Medulla and Cord. 

In addition to the degeneration in the nuclei of the 
posterior columns there is a scattered degeneration in the 
pyramids, restiform bodies and inter-olivary couch. 

Throughout the cord a degeneration similar to that seen 
in the medulla is shown by the Marchi method in the 
crossed and direct pyramidal tracts. The total number of 
degenerative fibres is but few and is less the lower down the 
cord is examined. 

In the anterior columns throughout the entire length of 
the cord there is a well-marked but scattered degeneration 
seen in sections stained by Marchi’s method. In the middle 
of the cord this degeneration becomes grouped in two 
positions, viz., that occupying the posterior portion of the 
column and that bounding the anterior and mesial borders; 
the former decreases as you descend and increases as you 
ascend the cord and is the direct pyramidal tract, whilst the 
anterior group, more marked than the posterior in the 
sacral region, becomes more extensive higher up the cord 
and spreads into the lateral columns. This degeneration 
probably consists of those fibres of the ventro-lateral efferent 



tract which have perished ; a corresponding degeneration 
in the angle between the corpus restiformi and the olive is 
not seen. 

In the anterior commissure degenerated fibres are seen 
by the Marchi method throughout the whole length of the 
cord; more especially is this seen in the region of L. 1 and 
D. 1. Several fibres seem to be definitely related to the 
direct pyramidal fibres in the anterior column. 

Very marked sclerosis is seen in Clarke’s column in the 
regions of the cord from L. 2 to D. 7; from here upwards 
the sclerosis becomes progressively less. Sections stained 
by Marchi’s method of the lower portion of this column 
show an abundance of fine, black dots in the network 
surrounding the ganglion cells. 

In some of the cells of Clarke’s column the nucleus is 
laterally displaced or dislocated. In the regions of D. 7 and 
D. 4 no such degenerated cells were noticed, but in the 
regions of L. 2, D. 1 and C. 8 several were observed, that is 
to say, that the cells of the column are affected at those 
regions of the cord which are in relation to the limbs. 

The Marchi method shows some degeneration in the 
anterior horns, which is very much more marked in the 
lumbar and sacral regions than elsewhere. In several 
sections fine rows of dots are seen in the course of fibres 
running in various directions through the horn. This de¬ 
generation in the anterior horn and the co-existence of 
degeneration in the ventro-lateral efferent tract is of especial 
interest in relation to the communication made by Professor 
Schafer to the Neurological Society at a recent meeting, in 
which he produced evidence to show that the termination of 
the ventro-lateral efferent tract takes place amongst the cells 
in the anterior horn. 

Examination of the Afferent Tracts Outside the 


The peripheral nerves in this case were, unfortunately, 
not preserved. The posterior roots of several segments 
were, however, examined and ganglia from various parts 



of the cord were stained by Marchi’s method and transverse 
sections from their distal and central ends compared. 
Frequent use was made of the Marchi-Pal method of 
staining. The posterior roots of the sacral and lower 
lumbar segments were found very markedly sclerosed; this 
sclerosis was still very evident in the roots of the 2nd lumbar 
and 12th dorsal nerve. The comparison of the distal and 
proximal ends of the ganglia proved, however, to be a very 
much more striking method of demonstrating the degenera¬ 
tion of the posterior roots. The great contrast between the 
healthy anterior and the degenerated posterior roots shown 
by the Marchi-Pal preparation is not more striking than 
that between the central and distal ends of the ganglia. 
This contrast is seen in all the ganglia examined, viz., L. 4, 
L. 2, D. 12, D. 10, D. 8, D. 5, C. 8, C. 6 and C. 2. 

The degeneration in the posterior root of the lumbar is 
not very much greater relatively to the size of the nerve 
than that seen in the dorsal region where, indeed, between 
the segments of D. 10 and 5 the posterior roots appear to 
suffer more change than elsewhere (diagram I., figs. 1 and (2. 
In the region of C. 8 a very considerable degeneration of the 
posterior roots is present, which diminishes in extent in the 
higher cervical roots, and is only just evident at the level of 
C. 2. In the distal ends of ganglia L. 4 and 2 there is 
some evidence of a very slight sclerosis, suggesting perhaps 
that had the peripheral nerves been examined some change 
might have been found in them. 

A comparison of diagram I. with the account given of the 
sclerosis in the posterior roots (photomicros. 1 and 2) is of 
some interest. The central mass of sclerosis in the pos¬ 
terior columns as far as D. 12 represents the diseased 
sensory neurons related to the lower limb. This mass 
whilst diminishing as it ascends, becomes concentrated in 
Goll’s columns. In figs. 10 to 14 there is seen to be a well- 
marked degeneration in the root zones which corresponds 
with the definite changes seen in the sections from the 
central ends of the dorsal ganglia (diagram I.). It is, more¬ 
over, especially interesting in view of the fact that the 
patient suffered from gastric crises. At the level of D. 1 and 


tion in • '.yolnm.iwcmfe. and cpnesponds witli the 

changes founh-it} the central'cud oi the Nth cervical gah^iisv, . 
Tim sudden increase of sclerosis represents the degenerated 

Fit* i. 

• ‘->j.,, •;• , -\ .•■/■.;•. f r i • M.c 

• j>»v * < ,’-\ • v^-'A* •VEW, . • f • % v v'-V-v i,* 



Figs. 1 and 2. -E’sampk*^ >A £0$ M: wtmiii Uvr> onetfr. Fig, 1- 

Tbia cell is not otherwise ttfom>rm&lL Kig. is yerV smirked dislocation 

af botli nucleu 

,. ■ 

■ ■ 


The. following, ganglia were. preserved in alcohol and. 
stained by' Nissts. metlj.mi and also by hauimtoxylin and 
Van Giessen : CI S, right and left; C '&.% l t D. 4., D. (J, 
L. 1, L. S', left and right; and b 5. Other ganglia. vbj., 
a ‘2. c; 7, and 0,8; l> 5, D 8, lb 10, D. 3 •£,. L. :i, L. 4 

nrr.viji <fv . i **, jfifl lit* /v i V t-'- VtVi-.t'iv/vid n tkcil r; f iV'f n it.' _ I 

stained by Weigert’s method. N cubing definite can be said 
oh tbs appearances seen jo the bodies of ihe-ganglia stained 

'•■vs ••'; * S- m ';' . > *«.'••■>•••'•'•'•■•' ; iVf'y'Y ■ • :< \i t : •.•'••.-•'.V':'' . • .,•*• ■ ... . :. ., - v-; y> i;A« '■> ill >V.-' ,4 V 1 '• 

In all ganglia examined the quantity of Abies stained by 
haniia.toxylui is markedly less towards the centra] than 
towarda the peripheral end. Th is feature is .Bspdcia^ly 'w.itll 
marked m the lumbar and dorsal region * and suggests that 

•; < V.V%,K-yrCr.-;vVy:' ?. ■ 

V^moyturuiH.Huni U. 

ul ral tiJiil </{ Ibe SiJi dorsal "giwg*inji), stiatyMig ^trophy of tile) 

poster lor roots. 

' illtpTOartoti.ofi&M’a 

Tit* f«s , )pi>ot*vl «ict ©C the ^TigUod. a>. VirtfcftVs 



the atrophy of the central prolongation of the sensory 
neurons has reached nearly, if not absolutely, to its trophic 

In no preparation could any evidence whatever of fibrosis 
of the ganglion be found. That sclerosis of nerve takes 
place is certain, but in this case of tabes no replacement of 
nerve tissue in the ganglia by excessive overgrowth of fibrous 
tissue has occurred. There is, however, an overgrowth of 
neuroglia cells which is figured in illustration II., and which 




. F 

CSfe •... ...j 

Mr .* 

L'^Ur ill.L 

I. lr >> 

R ft r\ dti 

Illustration II. 

A group of cells in the left third lumbar ganglion. All the cells shown 
are more or less wasted, and the peri-cellular lymph spaces are enlarged. 

A. —Cell showing marked dislocation of its nucleus. 

B. —Cell showing a similar change. 

C. —A cell which has stained very deeply; the nucleus has also taken on 
a deeper stain than normal. 

D. —Cell contents partially vacuolated; nucleus not differentiated from 
cell protoplasm; nucleolus deeply stained. 

E. —Cell showing more advanced changes of the same character. 

E . —Nucleolus appears to be discharging a nucleolar body. 

F. —Cell showing pigment and partial dislocation of nucleus. 

G. —A relatively healthy cell with some pigment. 

H. —A cell in which the nucleus has not been cut. 

I. —Overgrowth of neuroglia cells. 

appears in the preparations stained by Nissl’s method as a 
collection of cells with large ovoid vesicular nuclei and minute 



nucleoli, identical with those composing the capsules of the 
ganglion cells. Such an overgrowth is more marked in the 
lumbar region than elsewhere, but even here it is by no 
means a prominent feature. 

The changes seen in the cells of the posterior spinal 
ganglia by Nissl’s method are of two kinds; first, there is a 
general wasting of the cell body by reason of which the cell 
outline becomes very irregular, and the peri-cellular lym¬ 
phatic space much increased ; and secondly, a degeneration 
of the cell protoplasm which expresses itself by the phe¬ 
nomena of vacuolation of the protoplasm and dislocation of 
the nucleus. That the retraction of the cell is not an 
artefact is proved by the fact that in those cells where this 
exaggeration of the lymph space is not seen, no abnormality 
and generally no pigment can be observed in the cell body, 
whilst the examination of ganglia removed under identical 
conditions from normal bodies and from cases in which these 
structures are not involved shewed no such shrinkage. 

The various forms of change seen in the cells of the 
ganglia are great. A typical group is represented in illustra¬ 
tion II. The most striking change is the dislocation of the 
nucleus; this proceeds to such a degree that in many cells two- 
thirds of the nucleus may be freely projecting into the lymph 
space surrounded only by its own nuclear membrane. Com¬ 
plete separation of the nucleus and cell was not observed; 
presumably before this could occur the cell would have died 
and been removed in the lymph stream. It is surprising, 
however, how very few empty spaces are to be seen in any 
of the ganglia, and where they do occur they are no doubt 
due to the accidental dropping out of the cell in the course 
of the preparation of the section. In the 3rd lumbar 
ganglion, where perhaps the changes are most marked, there 
is a considerable overgrowth of neuroglia tissue which is 
probably derived from those capsules from which the cell 
body has been lost during the course of the disease. 

Vacuolation of the cell protoplasm is in many cells 
correlated with some nuclear change, more especially with 
the disappearance of the nuclear membrane, the appearance 
being that of a solution of the body of the nucleus. In such 



cases, however, the nucleolus is not only still persistent, but is 
even more marked than is normal (illustration II., D. and E.). 
In the cell marked E. such changes are very advanced, and 
in this cell what appears to be the dislocation of a nucleolar 
body from the nucleolus is evident (illustration II., E.). 
The granules stained blue by Nissl’s method appear to 
melt away and be replaced by a substance staining more 

In many cells vacuolation of the cell protoplasm occurs 
at some definite spot, and is related to the pigment which is 
there deposited in the cell, the cell body as a whole and its 
nucleus appearing relatively healthy. 

Certain cells take on a very deep blue by the Nissl 
method, although other cells in their immediate neighbour¬ 
hood are in no way over-stained. The granules cannot be 
differentiated towards the centre of the cell, and the nucleus 
is also much darker than usual; such cells, however, gener¬ 
ally are otherwise healthy in appearance. Whether it is an 
early stage of degeneration or an artefact is difficult to deter¬ 
mine (illustration II., C.). 

The greatest deflection from the normal was seen in 
ganglion L. 3, but the changes which have been described 
are present in all the other ganglia examined. In ganglion 
D. 1 there is a greater quantity of abnormal cells than 
in ganglion D. 4, although in the latter and ganglion D. 6 
there are still many. In ganglion C. 7 there appear to be 
fewer altered cells than in ganglion D. 1, whilst in ganglion 
C. 3 there are fewer than in ganglion C. 7. 

A typical longitudinal section of ganglion L. 3 was 
chosen, and a complete drawing was made of it on a large 
scale in which every cell was shown. The total number of 
cells present amounted to 816. Of these 17 5 per cent, 
contained pigment. Of the 675 cells which remained after 
deducting all those cells in which a nucleus was not cut, 12 
per cent, showed more or less marked dislocation of the 
nucleus. No special grouping of these altered cells could be 
made out. 

Reviewing the changes in the cells of the ganglia, as a 
whole, the degeneration seen in the cells and the structure 



of the ganglion are very much less marked than the changes 
in the posterior roots issuing from these ganglia. The 
presence of the limbs seems to have a corresponding effect 
on the ganglia of the nerves related to them to that seen 
in the corresponding portion of the spinal cord. Thus the 
ganglia L. 5 and L. 3, D. 1 and C. 7 show greater changes 
than those in the trunk region. 

It may be here mentioned that no changes in the vessels 
were observed which would account for the degenerative 
process. The walls of the vessels were not thickened 
generally, nor was there any sign of endarteritis. 

In the 3rd cervical right ganglion the examination of the 
few sections which were preserved brought out a very 
interesting fact. In two of these sections six examples were 
discovered of cells containing two nuclei with nucleoli. In 
consequence of this observation the ganglion of the left 
side was cut serially. In 176 sections twenty cells were 
discovered containing double nuclei. These cells could be 
traced in series and no evidence of their ultimate division 
was found. The majority of these cells, except for the 
presence of the two nuclei, appeared perfectly normal 
(page 396, figs. 1 and 2). The cell pictured on page 396, 
fig. 3, shows, however, in a most marked degree dislocation 
of both its nuclei. Some of these cells contained pigment 
(page 396, fig. 2); in no cell, however, is there any evidence 
of karyokinesis. Dr. Gaskell has suggested that these cells 
might possibly have a developmental significance in relation 
to the outgrowth of the sympathetic ganglia in the lower re¬ 
gions of the cord from the posterior spinal ganglia and that 
their occurrence in the 3rd cervical ganglia and in no other of 
those examined lower down is of interest, in view of the 
absence of segmented sympathetic ganglia in the cervical 

This observation has persuaded me to follow a suggestion 
given me by Dr. Mott that in cases of tabes, especially 
those in which gastric and bladder crises are well marked, 
the sympathetic system should be examined in the light 
of new methods. I am now collecting material for this 




My thanks are due to the Asylums Committee of the 
London County Council for permission to work in their 
laboratory at Claybury. I have the greatest pleasure in 
expressing my obligation to Dr. Mott for permitting me to 
use the material described and for much kind help in the 
course of this investigation. 



(Grocers' Research Scholar). 

(From the Pathological Laboratories of the University of Cambridge 
and of the London County Council.) 

Last autumn Dr. Mott suggested to me that I should 
make some researches upon the causation of that fatal bane 
of asylums known as Asylum Dysentery or Colitis; at the 
same time he offered to place the resources of the Laboratory 
of the London County Council at my service for the purpose. 
Somewhat later an outbreak of the disease occurred at the 
Claybury Asylum, which afforded the material for the obser¬ 
vations which form the subject of the present communi¬ 
cation. The enquiry was directed in two ways, (1) to search 
for a peculiar organism in the organs of fatal cases, which, 
as shewn hereafter, was successful; and (2) to try the effect 
of the blood-serum of those who had suffered for agglu¬ 
tinating effect upon known organisms. This method proved 

(1 )—Observations conducted with a view to the discovery of a 
specific micro-organism. 

Altogether eight cases were used for making cultivations; 
in seven of these one or more pure growths of a hitherto 
unknown micrococcus were obtained; these cases, with a 
few others, were also examined by microscopical methods, 
whereby the presence of the same organism could be made 
out. Furthermore, cultivations were made from the organs 
of three other patients who died from other causes; these 



failed to shew the presence of the above-mentioned micro¬ 
coccus, and formed controls. Upon the evidence thus 
afforded, I think that I am justified in considering that the 
micrococcus has an etiological significance; in the first 
place, it is an organism which could not be confounded with 
any other known micrococcus; in the second place it was 
found in a state of purity in one or other organ in the 
dysentery corpses examined, whilst it was absent in corpses 
of those dying of .other diseases, nor has it been described 
by other authors in this or other conditions; lastly, there 
are reasons why the micrococcus has not been recognised 
by former enquirers, viz., its exceedingly minute size and 
the difficulty with which growths on artificial media are 

Distribution of the micrococcus. —Pure cultures have been 
obtained from the blood, spleen, liver, kidney and bile. No 
cultivation experiments were made upon the stools passed 
during life; indeed, in general it may be stated that the bowel 
is about the last place to examine in any infective “ intestinal 
disease.” The chances of fallacy and the difficulty of dis¬ 
criminating between the hosts of different bacteria being 
very great. The mesenteric and colic lymphatic glands 
were disappointing from the cultural point of view, as they 
were almost invariably found to be infected with coli-like 
and other intestinal microbes. 

It will be observed that if the micrococcus is truly the 
cause of the dysentery, this disease is not one which is 
localised purely in the intestine. It is a general infection 
of the whole system, and, as in enteric fever, the changes 
in the bowel are perhaps to be regarded as more or less 
secondary in nature. 

Whatever be the nature of the action of the micrococcus 
or its poisonous products, it is clear that they have an 
affinity for the mucous membrane of the larger bowel. It 
is perhaps significant that, according to the notes kindly 
supplied to me by Dr. Orange, a number of the patients are 
recorded as being ill several days before the “ onset of the 

Morphological characters of the micrococcus. —It is an 



exceedingly minute body, and being near the border-line 
between the visible and the invisible, it is difficult to de¬ 
termine its shape accurately; as far as can be made out it is 
spherical. In cultivations the cocci are mostly single, some 
pairs, however, are to be seen specially during active growth; 
occasionally small chains of several individuals have been 
seen. It is sometimes difficult to determine whether certain 
forms are short chains of cocci or are of bacillary nature. 
In these respects it somewhat resembles the micro¬ 
coccus melitensis, but it is to be remembered that our 

Fio. 1 

Sketch of a specimen of mixed drops of cultures of pneumococcus and of 
the small micrococcus; the larger bodies are pneumococci. 

coccus is less than half the size of that organism. In 
old cultures, they may be clustered together in more or 
less flocculent masses, upon staining only here and there 
amongst the masses are stained individuals to be found. 
As would be expected in so small an organism, very active 
Brownian movements are to be seen; actual self-movement 
I have not been able to detect (no successful attempts have 
been made to demonstrate flagella, on account of the failure 
to obtain growths upon solid media). 



It may be stained by ordinary staining fluids, such as 
Kiihne’s carbol-blue, or weak watery methyl violet; in coverslip 
films (culture or juice of organs) staining by means of the 
Gram-Weigert method is successful; however, decolorisation 
must not be carried too far, and even then only a propor¬ 
tion of the cocci retain the stain. In sections of organs the 
chief difficulty is to differentiate the cocci from minute 
basophil granules. I find that the best method is to stain 
some sections by means of Pfeiffer’s method (weak carbol- 
fuchsin followed by highly dilute acetic acid) whereby both 
cocci and granules are stained red, and other sections with 
watery tliionin, whereby the cocci become deep blue, whilst 
the granules take on a reddish or violet colour. 

Probably owing to the action of alcohol in hardening, 
neither Gram-Weigert nor Nicolle’s acetone method is 
capable of shewing the cocci in sections of hardened tissue; 
by these means the presence of abundant fibrin network in 
the mucous and submucous layers of the colon are well 
shewn in the acute stage. 

Cultivation .—Microscopic examination of tissues would 
not have led to any satisfactory recognition of the micro¬ 
coccus without the assistance which is afforded by cultural 
methods. The micrococcus, however, does not grow at all 
freely in artificial media; hitherto it has only been grown 
in liquid media. All attempts to cultivate it upon solid media 
have been fraught with failure. Although it is not difficult to 
obtain original cultures from the organs, yet it is not easy to 
obtain sub-cultures, for, as a rule, the tubes which are thus 
inoculated remain permanently sterile. The easiest source 
for original culture is the bile. A few drops Of bile taken 
with a sterile capillary through the well-seared wall of the 
gall-bladder and planted in a tube of ordinary broth has 
uniformly yielded me pure cultures of the micrococcus. 
After three or four days’ incubation at body temperature the 
broth becomes faintly clouded. This cloud becomes more 
marked in a few more days. Microscopically it is found to 
be due to the minute micrococcus. In making cultures from 
other organs, it is necessary to take considerable quantities 
of the pulp of the organ. I used a large loop (about J 



inch long by £ inch wide) of thick platinum wire; one or 
two loopfuls were taken after thoroughly searing the surface 
of the organ with a red-hot instrument. Cultures which 
have been laid by taking a loopful with the ordinary small 
loops have been uniformly unsuccessful. 

I suppose that the reason of this is partly that only a 
small proportion of the cocci are able to survive transplanta¬ 
tion, and possibly the organ juice is a necessary factor in the 
constitution of the medium in which they grow outside the 
body for the first time. Be that as it may, it is necessary 
to transplant considerable quantities of the organ to be in¬ 
vestigated. In three to five days, or sometimes earlier, after 
inoculation of a broth tube with kidney, liver, or spleen of a 
dysentery patient, the broth will be found to have become 
clouded, the cloudiness being due to the presence of an 
extremely minute micrococcus. 

Sub-culture. —The majority of the attempts to obtain 
sub-cultivations from the primary pure cultivations have 
been attended with failure, although a considerable number 
of different media have been utilised. 

The best results so far have been obtained with yeast 
broth (Spronck). 1 When inoculated with a loopful or two of 
a pure culture this medium may show slight turbidity after a 
few days’ incubation, later resulting in a light, floccular mass, 
which settles to the bottom of the fluid. Some success has 
also been obtained by the addition of a few drops of sterile 
bile to ordinary broth. A series of generations has not yet 
been obtained. 

Transplantation of a single loopful of a cultivation which 
is full of the cocci in a state of division into ordinary broth 
has been invariably negative, for no growth whatever re¬ 
sults. Of the various media which have been tried the 
following may be mentioned:—Ordinary peptone broth 
(beef and pork), both with and without glycerin; broth 
made from freshly peptonised meat (with trypsin or 
L. Martin’s pig paunch broth); ascites broth; nutrose- 
ascites broth (Wasserman) 2 ; nutrose-serum broth ; liquid 

1 Ann . de VInst. Pasteur , 1898. 

• Zeitschr. f. Hygiene, xxvii., 1898. 



serum, either pure or with the addition of broth, or broth 
and blood, have all failed to yield growth when inoculated 
from the primary cultures. Thinking that possibly the 
fault might be in the reaction of the broth, I made a series 
of different alkalinities and acidities by adding graduated 
quantities of decinormal soda or acid to ordinary broth, but 
here again no success was obtained. 

It is clear that the presence of haemoglobin is not a 
necessity, as is the case with the influenza bacillus; also that 
an anaerobic condition is not a suitable environment, for 
growth in Buchner tubes was either scanty or absent; the 
latter was also the case in broth to which small quantities 
of sodium sulphide had been added (Trenkmann) 1 . Media 
solidified with agar corresponding to the abov